[{"author":[{"first_name":"José","last_name":"Guzmán","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","full_name":"Guzmán, José"},{"last_name":"Schlögl","first_name":"Alois","orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","full_name":"Schlögl, Alois"},{"full_name":"Frotscher, Michael","first_name":"Michael","last_name":"Frotscher"},{"full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","first_name":"Peter M"}],"volume":353,"date_updated":"2021-01-12T06:50:04Z","date_created":"2018-12-11T11:51:31Z","year":"2016","publisher":"American Association for the Advancement of Science","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"publication_status":"published","ec_funded":1,"publist_id":"5899","file_date_updated":"2020-07-14T12:44:46Z","doi":"10.1126/science.aaf1836","language":[{"iso":"eng"}],"acknowledged_ssus":[{"_id":"ScienComp"}],"oa":1,"project":[{"call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548"},{"call_identifier":"FWF","name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"}],"quality_controlled":"1","month":"09","pubrep_id":"823","file":[{"content_type":"application/pdf","file_size":19408143,"creator":"system","access_level":"open_access","file_name":"IST-2017-823-v1+1_aaf1836_CombinedPDF_v2-1.pdf","checksum":"89caefa4e181424cbf0aecc835fcc5ec","date_updated":"2020-07-14T12:44:46Z","date_created":"2018-12-12T10:12:27Z","relation":"main_file","file_id":"4945"}],"oa_version":"Preprint","_id":"1350","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":" 353","ddc":["570"],"status":"public","title":"Synaptic mechanisms of pattern completion in the hippocampal CA3 network","issue":"6304","abstract":[{"lang":"eng","text":"The hippocampal CA3 region plays a key role in learning and memory. Recurrent CA3–CA3\r\nsynapses are thought to be the subcellular substrate of pattern completion. However, the\r\nsynaptic mechanisms of this network computation remain enigmatic. To investigate these mechanisms, we combined functional connectivity analysis with network modeling.\r\nSimultaneous recording fromup to eight CA3 pyramidal neurons revealed that connectivity was sparse, spatially uniform, and highly enriched in disynaptic motifs (reciprocal, convergence,divergence, and chain motifs). Unitary connections were composed of one or two synaptic contacts, suggesting efficient use of postsynaptic space. Real-size modeling indicated that CA3 networks with sparse connectivity, disynaptic motifs, and single-contact connections robustly generated pattern completion.Thus, macro- and microconnectivity contribute to efficient\r\nmemory storage and retrieval in hippocampal networks."}],"type":"journal_article","date_published":"2016-09-09T00:00:00Z","citation":{"short":"J. Guzmán, A. Schlögl, M. Frotscher, P.M. Jonas, Science 353 (2016) 1117–1123.","mla":"Guzmán, José, et al. “Synaptic Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” Science, vol. 353, no. 6304, American Association for the Advancement of Science, 2016, pp. 1117–23, doi:10.1126/science.aaf1836.","chicago":"Guzmán, José, Alois Schlögl, Michael Frotscher, and Peter M Jonas. “Synaptic Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” Science. American Association for the Advancement of Science, 2016. https://doi.org/10.1126/science.aaf1836.","ama":"Guzmán J, Schlögl A, Frotscher M, Jonas PM. Synaptic mechanisms of pattern completion in the hippocampal CA3 network. Science. 2016;353(6304):1117-1123. doi:10.1126/science.aaf1836","ieee":"J. Guzmán, A. Schlögl, M. Frotscher, and P. M. Jonas, “Synaptic mechanisms of pattern completion in the hippocampal CA3 network,” Science, vol. 353, no. 6304. American Association for the Advancement of Science, pp. 1117–1123, 2016.","apa":"Guzmán, J., Schlögl, A., Frotscher, M., & Jonas, P. M. (2016). Synaptic mechanisms of pattern completion in the hippocampal CA3 network. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aaf1836","ista":"Guzmán J, Schlögl A, Frotscher M, Jonas PM. 2016. Synaptic mechanisms of pattern completion in the hippocampal CA3 network. Science. 353(6304), 1117–1123."},"publication":"Science","page":"1117 - 1123","has_accepted_license":"1","day":"09","scopus_import":1},{"quality_controlled":"1","oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"language":[{"iso":"eng"}],"doi":"10.1155/2016/1207393","month":"01","publisher":"Hindawi Publishing Corporation","department":[{"_id":"PeJo"}],"publication_status":"published","year":"2016","volume":2016,"date_updated":"2021-01-12T06:50:43Z","date_created":"2018-12-11T11:52:00Z","author":[{"last_name":"Guzmán","first_name":"José","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","full_name":"Guzmán, José"},{"last_name":"Gerevich","first_name":"Zoltan","full_name":"Gerevich, Zoltan"}],"article_number":"1207393","license":"https://creativecommons.org/licenses/by/4.0/","publist_id":"5762","file_date_updated":"2020-07-14T12:44:54Z","citation":{"ista":"Guzmán J, Gerevich Z. 2016. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. 2016, 1207393.","apa":"Guzmán, J., & Gerevich, Z. (2016). P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. Hindawi Publishing Corporation. https://doi.org/10.1155/2016/1207393","ieee":"J. Guzmán and Z. Gerevich, “P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction,” Neural Plasticity, vol. 2016. Hindawi Publishing Corporation, 2016.","ama":"Guzmán J, Gerevich Z. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. 2016;2016. doi:10.1155/2016/1207393","chicago":"Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” Neural Plasticity. Hindawi Publishing Corporation, 2016. https://doi.org/10.1155/2016/1207393.","mla":"Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” Neural Plasticity, vol. 2016, 1207393, Hindawi Publishing Corporation, 2016, doi:10.1155/2016/1207393.","short":"J. Guzmán, Z. Gerevich, Neural Plasticity 2016 (2016)."},"publication":"Neural Plasticity","date_published":"2016-01-01T00:00:00Z","scopus_import":1,"has_accepted_license":"1","day":"01","intvolume":" 2016","title":"P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction","status":"public","ddc":["570"],"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","_id":"1435","file":[{"file_name":"IST-2016-580-v1+1_1207393.pdf","access_level":"open_access","creator":"system","content_type":"application/pdf","file_size":1395180,"file_id":"4740","relation":"main_file","date_updated":"2020-07-14T12:44:54Z","date_created":"2018-12-12T10:09:17Z","checksum":"8dc5c2f3d44d4775a6e7e3edb0d7a0da"}],"oa_version":"Published Version","pubrep_id":"580","type":"journal_article","abstract":[{"text":"ATP released from neurons and astrocytes during neuronal activity or under pathophysiological circumstances is able to influence information flow in neuronal circuits by activation of ionotropic P2X and metabotropic P2Y receptors and subsequent modulation of cellular excitability, synaptic strength, and plasticity. In the present paper we review cellular and network effects of P2Y receptors in the brain. We show that P2Y receptors inhibit the release of neurotransmitters, modulate voltage- and ligand-gated ion channels, and differentially influence the induction of synaptic plasticity in the prefrontal cortex, hippocampus, and cerebellum. The findings discussed here may explain how P2Y1 receptor activation during brain injury, hypoxia, inflammation, schizophrenia, or Alzheimer's disease leads to an impairment of cognitive processes. Hence, it is suggested that the blockade of P2Y1 receptors may have therapeutic potential against cognitive disturbances in these states.","lang":"eng"}]},{"language":[{"iso":"eng"}],"conference":{"name":"AHPC: Austrian HPC Meeting","end_date":"2016-02-24","start_date":"2016-02-22","location":"Grundlsee, Austria"},"date_published":"2016-02-24T00:00:00Z","quality_controlled":"1","page":"37","publication":"AHPC16 - Austrian HPC Meeting 2016","oa":1,"citation":{"mla":"Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST Austria: Modelling the Human Hippocampus.” AHPC16 - Austrian HPC Meeting 2016, VSC - Vienna Scientific Cluster, 2016, p. 37.","short":"A. Schlögl, S. Stadlbauer, in:, AHPC16 - Austrian HPC Meeting 2016, VSC - Vienna Scientific Cluster, 2016, p. 37.","chicago":"Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST Austria: Modelling the Human Hippocampus.” In AHPC16 - Austrian HPC Meeting 2016, 37. VSC - Vienna Scientific Cluster, 2016.","ama":"Schlögl A, Stadlbauer S. High performance computing at IST Austria: Modelling the human hippocampus. In: AHPC16 - Austrian HPC Meeting 2016. VSC - Vienna Scientific Cluster; 2016:37.","ista":"Schlögl A, Stadlbauer S. 2016. High performance computing at IST Austria: Modelling the human hippocampus. AHPC16 - Austrian HPC Meeting 2016. AHPC: Austrian HPC Meeting, 37.","apa":"Schlögl, A., & Stadlbauer, S. (2016). High performance computing at IST Austria: Modelling the human hippocampus. In AHPC16 - Austrian HPC Meeting 2016 (p. 37). Grundlsee, Austria: VSC - Vienna Scientific Cluster.","ieee":"A. Schlögl and S. Stadlbauer, “High performance computing at IST Austria: Modelling the human hippocampus,” in AHPC16 - Austrian HPC Meeting 2016, Grundlsee, Austria, 2016, p. 37."},"main_file_link":[{"url":"https://vsc.ac.at/fileadmin/user_upload/vsc/conferences/ahpc16/BOOKLET_AHPC16.pdf","open_access":"1"}],"day":"24","month":"02","article_processing_charge":"No","has_accepted_license":"1","date_updated":"2023-05-16T07:15:14Z","date_created":"2023-05-05T12:54:47Z","oa_version":"Published Version","file":[{"relation":"main_file","file_id":"12968","date_created":"2023-05-16T07:03:56Z","date_updated":"2023-05-16T07:03:56Z","checksum":"4a7b00362e81358d568f5e216fa03c3e","success":1,"file_name":"2016_AHPC_Schloegl.pdf","access_level":"open_access","file_size":1073523,"content_type":"application/pdf","creator":"dernst"}],"author":[{"full_name":"Schlögl, Alois","last_name":"Schlögl","first_name":"Alois","orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Stadlbauer","first_name":"Stephan","id":"4D0BC184-F248-11E8-B48F-1D18A9856A87","full_name":"Stadlbauer, Stephan"}],"title":"High performance computing at IST Austria: Modelling the human hippocampus","status":"public","ddc":["000"],"publication_status":"published","publisher":"VSC - Vienna Scientific Cluster","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"_id":"12903","year":"2016","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file_date_updated":"2023-05-16T07:03:56Z","type":"conference_abstract"},{"author":[{"full_name":"Mishra, Rajiv Kumar","id":"46CB58F2-F248-11E8-B48F-1D18A9856A87","first_name":"Rajiv Kumar","last_name":"Mishra"},{"full_name":"Kim, Sooyun","id":"394AB1C8-F248-11E8-B48F-1D18A9856A87","first_name":"Sooyun","last_name":"Kim"},{"orcid":"0000-0003-2209-5242","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","last_name":"Guzmán","first_name":"José","full_name":"Guzmán, José"},{"full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804"}],"related_material":{"record":[{"id":"1396","relation":"dissertation_contains","status":"public"}]},"date_created":"2018-12-11T11:51:59Z","date_updated":"2023-09-07T11:55:25Z","volume":7,"year":"2016","acknowledgement":"We thank Jozsef Csicsvari and Nelson Spruston for critically reading the manuscript. We also thank A. Schlögl for programming, F. Marr for technical assistance and E. Kramberger for manuscript editing. ","publication_status":"published","publisher":"Nature Publishing Group","department":[{"_id":"PeJo"}],"file_date_updated":"2020-07-14T12:44:53Z","publist_id":"5766","ec_funded":1,"article_number":"11552","doi":"10.1038/ncomms11552","language":[{"iso":"eng"}],"oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"quality_controlled":"1","project":[{"grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","name":"Mechanisms of transmitter release at GABAergic synapses","call_identifier":"FWF"},{"grant_number":"268548","_id":"25C0F108-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"}],"month":"05","pubrep_id":"582","oa_version":"Published Version","file":[{"content_type":"application/pdf","file_size":4510512,"creator":"system","file_name":"IST-2016-582-v1+1_ncomms11552.pdf","access_level":"open_access","date_updated":"2020-07-14T12:44:53Z","date_created":"2018-12-12T10:18:33Z","checksum":"7e84d0392348c874d473b62f1042de22","relation":"main_file","file_id":"5355"}],"_id":"1432","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","ddc":["570"],"title":"Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks","status":"public","intvolume":" 7","abstract":[{"lang":"eng","text":"CA3–CA3 recurrent excitatory synapses are thought to play a key role in memory storage and pattern completion. Whether the plasticity properties of these synapses are consistent with their proposed network functions remains unclear. Here, we examine the properties of spike timing-dependent plasticity (STDP) at CA3–CA3 synapses. Low-frequency pairing of excitatory postsynaptic potentials (EPSPs) and action potentials (APs) induces long-term potentiation (LTP), independent of temporal order. The STDP curve is symmetric and broad (half-width ~150 ms). Consistent with these STDP induction properties, AP–EPSP sequences lead to supralinear summation of spine [Ca2+] transients. Furthermore, afterdepolarizations (ADPs) following APs efficiently propagate into dendrites of CA3 pyramidal neurons, and EPSPs summate with dendritic ADPs. In autoassociative network models, storage and recall are more robust with symmetric than with asymmetric STDP rules. Thus, a specialized STDP induction rule allows reliable storage and recall of information in the hippocampal CA3 network."}],"type":"journal_article","date_published":"2016-05-13T00:00:00Z","publication":"Nature Communications","citation":{"chicago":"Mishra, Rajiv Kumar, Sooyun Kim, José Guzmán, and Peter M Jonas. “Symmetric Spike Timing-Dependent Plasticity at CA3–CA3 Synapses Optimizes Storage and Recall in Autoassociative Networks.” Nature Communications. Nature Publishing Group, 2016. https://doi.org/10.1038/ncomms11552.","mla":"Mishra, Rajiv Kumar, et al. “Symmetric Spike Timing-Dependent Plasticity at CA3–CA3 Synapses Optimizes Storage and Recall in Autoassociative Networks.” Nature Communications, vol. 7, 11552, Nature Publishing Group, 2016, doi:10.1038/ncomms11552.","short":"R.K. Mishra, S. Kim, J. Guzmán, P.M. Jonas, Nature Communications 7 (2016).","ista":"Mishra RK, Kim S, Guzmán J, Jonas PM. 2016. Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. Nature Communications. 7, 11552.","ieee":"R. K. Mishra, S. Kim, J. Guzmán, and P. M. Jonas, “Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks,” Nature Communications, vol. 7. Nature Publishing Group, 2016.","apa":"Mishra, R. K., Kim, S., Guzmán, J., & Jonas, P. M. (2016). Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms11552","ama":"Mishra RK, Kim S, Guzmán J, Jonas PM. Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. Nature Communications. 2016;7. doi:10.1038/ncomms11552"},"day":"13","has_accepted_license":"1","scopus_import":1},{"year":"2016","publisher":"Institute of Science and Technology Austria","department":[{"_id":"PeJo"}],"publication_status":"published","related_material":{"record":[{"id":"1432","relation":"part_of_dissertation","status":"public"}]},"author":[{"id":"46CB58F2-F248-11E8-B48F-1D18A9856A87","first_name":"Rajiv Kumar","last_name":"Mishra","full_name":"Mishra, Rajiv Kumar"}],"date_updated":"2023-09-07T11:55:26Z","date_created":"2018-12-11T11:51:46Z","publist_id":"5811","file_date_updated":"2021-02-22T11:48:44Z","oa":1,"language":[{"iso":"eng"}],"degree_awarded":"PhD","supervisor":[{"full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804"}],"publication_identifier":{"issn":["2663-337X"]},"month":"03","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"1396","title":"Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus","status":"public","ddc":["570"],"file":[{"creator":"dernst","content_type":"application/pdf","file_size":2407572,"file_name":"Thesis_Mishra_Rajiv (Final).pdf","access_level":"closed","date_updated":"2020-07-14T12:44:48Z","date_created":"2019-08-09T12:14:46Z","checksum":"5a010a838faf040f7064f3cfb802f743","file_id":"6782","relation":"main_file"},{"date_updated":"2021-02-22T11:48:44Z","date_created":"2021-02-22T11:48:44Z","success":1,"checksum":"81b26d9ede92c99f1d8cc6fa1d04cbbb","file_id":"9183","relation":"main_file","creator":"dernst","file_size":2407572,"content_type":"application/pdf","file_name":"2016_RajivMishra_Thesis.pdf","access_level":"open_access"}],"oa_version":"Published Version","type":"dissertation","alternative_title":["ISTA Thesis"],"abstract":[{"lang":"eng","text":"CA3 pyramidal neurons are thought to pay a key role in memory storage and pattern completion by activity-dependent synaptic plasticity between CA3-CA3 recurrent excitatory synapses. To examine the induction rules of synaptic plasticity at CA3-CA3 synapses, we performed whole-cell patch-clamp recordings in acute hippocampal slices from rats (postnatal 21-24 days) at room temperature. Compound excitatory postsynaptic potentials (ESPSs) were recorded by tract stimulation in stratum oriens in the presence of 10 µM gabazine. High-frequency stimulation (HFS) induced N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP). Although LTP by HFS did not requier postsynaptic spikes, it was blocked by Na+-channel blockers suggesting that local active processes (e.g.) dendritic spikes) may contribute to LTP induction without requirement of a somatic action potential (AP). We next examined the properties of spike timing-dependent plasticity (STDP) at CA3-CA3 synapses. Unexpectedly, low-frequency pairing of EPSPs and backpropagated action potentialy (bAPs) induced LTP, independent of temporal order. The STDP curve was symmetric and broad, with a half-width of ~150 ms. Consistent with these specific STDP induction properties, post-presynaptic sequences led to a supralinear summation of spine [Ca2+] transients. Furthermore, in autoassociative network models, storage and recall was substantially more robust with symmetric than with asymmetric STDP rules. In conclusion, we found associative forms of LTP at CA3-CA3 recurrent collateral synapses with distinct induction rules. LTP induced by HFS may be associated with dendritic spikes. In contrast, low frequency pairing of pre- and postsynaptic activity induced LTP only if EPSP-AP were temporally very close. Together, these induction mechanisms of synaptiic plasticity may contribute to memory storage in the CA3-CA3 microcircuit at different ranges of activity."}],"citation":{"mla":"Mishra, Rajiv Kumar. Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus. Institute of Science and Technology Austria, 2016.","short":"R.K. Mishra, Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus, Institute of Science and Technology Austria, 2016.","chicago":"Mishra, Rajiv Kumar. “Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus.” Institute of Science and Technology Austria, 2016.","ama":"Mishra RK. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. 2016.","ista":"Mishra RK. 2016. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. Institute of Science and Technology Austria.","ieee":"R. K. Mishra, “Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus,” Institute of Science and Technology Austria, 2016.","apa":"Mishra, R. K. (2016). Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. Institute of Science and Technology Austria."},"page":"83","date_published":"2016-03-01T00:00:00Z","has_accepted_license":"1","article_processing_charge":"No","day":"01"},{"has_accepted_license":"1","article_processing_charge":"No","day":"01","scopus_import":"1","date_published":"2016-05-01T00:00:00Z","citation":{"chicago":"Kowalski, Janina, Jian Gan, Peter M Jonas, and Alejandro Pernia-Andrade. “Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern in Vivo in Anesthetized Rats.” Hippocampus. Wiley, 2016. https://doi.org/10.1002/hipo.22550.","short":"J. Kowalski, J. Gan, P.M. Jonas, A. Pernia-Andrade, Hippocampus 26 (2016) 668–682.","mla":"Kowalski, Janina, et al. “Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern in Vivo in Anesthetized Rats.” Hippocampus, vol. 26, no. 5, Wiley, 2016, pp. 668–82, doi:10.1002/hipo.22550.","ieee":"J. Kowalski, J. Gan, P. M. Jonas, and A. Pernia-Andrade, “Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats,” Hippocampus, vol. 26, no. 5. Wiley, pp. 668–682, 2016.","apa":"Kowalski, J., Gan, J., Jonas, P. M., & Pernia-Andrade, A. (2016). Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. Hippocampus. Wiley. https://doi.org/10.1002/hipo.22550","ista":"Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. 2016. Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. Hippocampus. 26(5), 668–682.","ama":"Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. Hippocampus. 2016;26(5):668-682. doi:10.1002/hipo.22550"},"publication":"Hippocampus","page":"668 - 682","issue":"5","abstract":[{"lang":"eng","text":"The hippocampus plays a key role in learning and memory. Previous studies suggested that the main types of principal neurons, dentate gyrus granule cells (GCs), CA3 pyramidal neurons, and CA1 pyramidal neurons, differ in their activity pattern, with sparse firing in GCs and more frequent firing in CA3 and CA1 pyramidal neurons. It has been assumed but never shown that such different activity may be caused by differential synaptic excitation. To test this hypothesis, we performed high-resolution whole-cell patch-clamp recordings in anesthetized rats in vivo. In contrast to previous in vitro data, both CA3 and CA1 pyramidal neurons fired action potentials spontaneously, with a frequency of ∼3–6 Hz, whereas GCs were silent. Furthermore, both CA3 and CA1 cells primarily fired in bursts. To determine the underlying mechanisms, we quantitatively assessed the frequency of spontaneous excitatory synaptic input, the passive membrane properties, and the active membrane characteristics. Surprisingly, GCs showed comparable synaptic excitation to CA3 and CA1 cells and the highest ratio of excitation versus hyperpolarizing inhibition. Thus, differential synaptic excitation is not responsible for differences in firing. Moreover, the three types of hippocampal neurons markedly differed in their passive properties. While GCs showed the most negative membrane potential, CA3 pyramidal neurons had the highest input resistance and the slowest membrane time constant. The three types of neurons also differed in the active membrane characteristics. GCs showed the highest action potential threshold, but displayed the largest gain of the input-output curves. In conclusion, our results reveal that differential firing of the three main types of hippocampal principal neurons in vivo is not primarily caused by differences in the characteristics of the synaptic input, but by the distinct properties of synaptic integration and input-output transformation."}],"type":"journal_article","pubrep_id":"469","file":[{"file_id":"5033","relation":"main_file","checksum":"284b72b12fbe15474833ed3d4549f86b","date_updated":"2020-07-14T12:45:07Z","date_created":"2018-12-12T10:13:47Z","access_level":"open_access","file_name":"IST-2016-469-v1+1_Kowalski_et_al-Hippocampus.pdf","creator":"system","content_type":"application/pdf","file_size":905348}],"oa_version":"Published Version","_id":"1616","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":" 26","title":"Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats","status":"public","ddc":["570"],"publication_identifier":{"eissn":["1098-1063"],"issn":["1050-9631"]},"month":"05","doi":"10.1002/hipo.22550","language":[{"iso":"eng"}],"tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png"},"oa":1,"quality_controlled":"1","publist_id":"5550","file_date_updated":"2020-07-14T12:45:07Z","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","author":[{"full_name":"Kowalski, Janina","last_name":"Kowalski","first_name":"Janina","id":"3F3CA136-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Gan, Jian","id":"3614E438-F248-11E8-B48F-1D18A9856A87","last_name":"Gan","first_name":"Jian"},{"last_name":"Jonas","first_name":"Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M"},{"last_name":"Pernia-Andrade","first_name":"Alejandro","id":"36963E98-F248-11E8-B48F-1D18A9856A87","full_name":"Pernia-Andrade, Alejandro"}],"volume":26,"date_created":"2018-12-11T11:53:03Z","date_updated":"2023-10-17T10:02:02Z","year":"2016","acknowledgement":"The authors thank Jose Guzman for critically reading prior versions of the manuscript. They also thank T. Asenov for\r\nengineering mechanical devices, A. Schlögl for efficient pro-gramming, F. Marr for technical assistance, and E. Kramberger for manuscript editing.","publisher":"Wiley","department":[{"_id":"PeJo"}],"publication_status":"published"},{"doi":"10.2174/1874467208666150507105443","language":[{"iso":"eng"}],"external_id":{"pmid":["25966692"]},"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384372/","open_access":"1"}],"oa":1,"quality_controlled":"1","month":"10","author":[{"full_name":"Vandael, David H","orcid":"0000-0001-7577-1676","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","last_name":"Vandael","first_name":"David H"},{"full_name":"Marcantoni, Andrea","first_name":"Andrea","last_name":"Marcantoni"},{"full_name":"Carbone, Emilio","last_name":"Carbone","first_name":"Emilio"}],"date_created":"2018-12-11T11:52:35Z","date_updated":"2021-01-12T06:51:26Z","volume":8,"year":"2015","acknowledgement":"This work was supported by the Italian MIUR (PRIN 2010/2011 project 2010JFYFY2) and the University of Torino.","pmid":1,"publication_status":"published","department":[{"_id":"PeJo"}],"publisher":"Bentham Science Publishers","publist_id":"5636","date_published":"2015-10-01T00:00:00Z","publication":"Current Molecular Pharmacology","citation":{"ista":"Vandael DH, Marcantoni A, Carbone E. 2015. Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. Current Molecular Pharmacology. 8(2), 149–161.","apa":"Vandael, D. H., Marcantoni, A., & Carbone, E. (2015). Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. Current Molecular Pharmacology. Bentham Science Publishers. https://doi.org/10.2174/1874467208666150507105443","ieee":"D. H. Vandael, A. Marcantoni, and E. Carbone, “Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells,” Current Molecular Pharmacology, vol. 8, no. 2. Bentham Science Publishers, pp. 149–161, 2015.","ama":"Vandael DH, Marcantoni A, Carbone E. Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. Current Molecular Pharmacology. 2015;8(2):149-161. doi:10.2174/1874467208666150507105443","chicago":"Vandael, David H, Andrea Marcantoni, and Emilio Carbone. “Cav1.3 Channels as Key Regulators of Neuron-like Firings and Catecholamine Release in Chromaffin Cells.” Current Molecular Pharmacology. Bentham Science Publishers, 2015. https://doi.org/10.2174/1874467208666150507105443.","mla":"Vandael, David H., et al. “Cav1.3 Channels as Key Regulators of Neuron-like Firings and Catecholamine Release in Chromaffin Cells.” Current Molecular Pharmacology, vol. 8, no. 2, Bentham Science Publishers, 2015, pp. 149–61, doi:10.2174/1874467208666150507105443.","short":"D.H. Vandael, A. Marcantoni, E. Carbone, Current Molecular Pharmacology 8 (2015) 149–161."},"article_type":"original","page":"149 - 161","day":"01","article_processing_charge":"No","scopus_import":1,"oa_version":"Submitted Version","_id":"1535","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","title":"Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells","intvolume":" 8","abstract":[{"text":"Neuronal and neuroendocrine L-type calcium channels (Cav1.2, Cav1.3) open readily at relatively low membrane potentials and allow Ca2+ to enter the cells near resting potentials. In this way, Cav1.2 and Cav1.3 shape the action potential waveform, contribute to gene expression, synaptic plasticity, neuronal differentiation, hormone secretion and pacemaker activity. In the chromaffin cells (CCs) of the adrenal medulla, Cav1.3 is highly expressed and is shown to support most of the pacemaking current that sustains action potential (AP) firings and part of the catecholamine secretion. Cav1.3 forms Ca2+-nanodomains with the fast inactivating BK channels and drives the resting SK currents. These latter set the inter-spike interval duration between consecutive spikes during spontaneous firing and the rate of spike adaptation during sustained depolarizations. Cav1.3 plays also a primary role in the switch from “tonic” to “burst” firing that occurs in mouse CCs when either the availability of voltage-gated Na channels (Nav) is reduced or the β2 subunit featuring the fast inactivating BK channels is deleted. Here, we discuss the functional role of these “neuronlike” firing modes in CCs and how Cav1.3 contributes to them. The open issue is to understand how these novel firing patterns are adapted to regulate the quantity of circulating catecholamines during resting condition or in response to acute and chronic stress.","lang":"eng"}],"issue":"2","type":"journal_article"},{"publist_id":"5606","acknowledgement":"This work was supported by the Compagnia di San Paolo Foundation ‘Neuroscience Program’ to VC and ‘Progetto di Ateneo 2011-13’ to EC.\r\nWe thank Dr Claudio Franchino for cell preparation and for providing excellent technical support.","year":"2015","pmid":1,"publication_status":"published","publisher":"Wiley-Blackwell","department":[{"_id":"PeJo"}],"author":[{"full_name":"Gavello, Daniela","first_name":"Daniela","last_name":"Gavello"},{"full_name":"Vandael, David H","orcid":"0000-0001-7577-1676","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","last_name":"Vandael","first_name":"David H"},{"last_name":"Gosso","first_name":"Sara","full_name":"Gosso, Sara"},{"last_name":"Carbone","first_name":"Emilio","full_name":"Carbone, Emilio"},{"first_name":"Valentina","last_name":"Carabelli","full_name":"Carabelli, Valentina"}],"date_updated":"2021-01-12T06:51:38Z","date_created":"2018-12-11T11:52:45Z","volume":593,"month":"11","external_id":{"pmid":["26282459"]},"oa":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650409/","open_access":"1"}],"quality_controlled":"1","doi":"10.1113/JP271078","language":[{"iso":"eng"}],"type":"journal_article","abstract":[{"text":"Leptin is an adipokine produced by the adipose tissue regulating body weight through its appetite-suppressing effect. Besides being expressed in the hypothalamus and hippocampus, leptin receptors (ObRs) are also present in chromaffin cells of the adrenal medulla. In the present study, we report the effect of leptin on mouse chromaffin cell (MCC) functionality, focusing on cell excitability and catecholamine secretion. Acute application of leptin (1 nm) on spontaneously firing MCCs caused a slowly developing membrane hyperpolarization followed by complete blockade of action potential (AP) firing. This inhibitory effect at rest was abolished by the BK channel blocker paxilline (1 μm), suggesting the involvement of BK potassium channels. Single-channel recordings in 'perforated microvesicles' confirmed that leptin increased BK channel open probability without altering its unitary conductance. BK channel up-regulation was associated with the phosphoinositide 3-kinase (PI3K) signalling cascade because the PI3K specific inhibitor wortmannin (100 nm) fully prevented BK current increase. We also tested the effect of leptin on evoked AP firing and Ca2+-driven exocytosis. Although leptin preserves well-adapted AP trains of lower frequency, APs are broader and depolarization-evoked exocytosis is increased as a result of the larger size of the ready-releasable pool and higher frequency of vesicle release. The kinetics and quantal size of single secretory events remained unaltered. Leptin had no effect on firing and secretion in db-/db- mice lacking the ObR gene, confirming its specificity. In conclusion, leptin exhibits a dual action on MCC activity. It dampens AP firing at rest but preserves AP firing and increases catecholamine secretion during sustained stimulation, highlighting the importance of the adipo-adrenal axis in the leptin-mediated increase of sympathetic tone and catecholamine release.","lang":"eng"}],"issue":"22","_id":"1565","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","status":"public","title":"Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells","intvolume":" 593","oa_version":"Submitted Version","scopus_import":1,"day":"15","publication":"Journal of Physiology","citation":{"ieee":"D. Gavello, D. H. Vandael, S. Gosso, E. Carbone, and V. Carabelli, “Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells,” Journal of Physiology, vol. 593, no. 22. Wiley-Blackwell, pp. 4835–4853, 2015.","apa":"Gavello, D., Vandael, D. H., Gosso, S., Carbone, E., & Carabelli, V. (2015). Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells. Journal of Physiology. Wiley-Blackwell. https://doi.org/10.1113/JP271078","ista":"Gavello D, Vandael DH, Gosso S, Carbone E, Carabelli V. 2015. Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells. Journal of Physiology. 593(22), 4835–4853.","ama":"Gavello D, Vandael DH, Gosso S, Carbone E, Carabelli V. Dual action of leptin on rest-firing and stimulated catecholamine release via phosphoinositide 3-kinase-riven BK channel up-regulation in mouse chromaffin cells. Journal of Physiology. 2015;593(22):4835-4853. doi:10.1113/JP271078","chicago":"Gavello, Daniela, David H Vandael, Sara Gosso, Emilio Carbone, and Valentina Carabelli. “Dual Action of Leptin on Rest-Firing and Stimulated Catecholamine Release via Phosphoinositide 3-Kinase-Riven BK Channel up-Regulation in Mouse Chromaffin Cells.” Journal of Physiology. Wiley-Blackwell, 2015. https://doi.org/10.1113/JP271078.","short":"D. Gavello, D.H. Vandael, S. Gosso, E. Carbone, V. Carabelli, Journal of Physiology 593 (2015) 4835–4853.","mla":"Gavello, Daniela, et al. “Dual Action of Leptin on Rest-Firing and Stimulated Catecholamine Release via Phosphoinositide 3-Kinase-Riven BK Channel up-Regulation in Mouse Chromaffin Cells.” Journal of Physiology, vol. 593, no. 22, Wiley-Blackwell, 2015, pp. 4835–53, doi:10.1113/JP271078."},"page":"4835 - 4853","date_published":"2015-11-15T00:00:00Z"},{"oa_version":"Submitted Version","file":[{"access_level":"open_access","file_name":"2015_Neuroscience_Brenes.pdf","creator":"dernst","content_type":"application/pdf","file_size":5563015,"file_id":"7849","relation":"main_file","checksum":"af2c4c994718c7be417eba0dc746aac9","date_created":"2020-05-15T06:50:20Z","date_updated":"2020-07-14T12:45:02Z"}],"_id":"1580","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","ddc":["570"],"status":"public","title":"Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons","intvolume":" 311","abstract":[{"text":"Synapsins (Syns) are an evolutionarily conserved family of presynaptic proteins crucial for the fine-tuning of synaptic function. A large amount of experimental evidences has shown that Syns are involved in the development of epileptic phenotypes and several mutations in Syn genes have been associated with epilepsy in humans and animal models. Syn mutations induce alterations in circuitry and neurotransmitter release, differentially affecting excitatory and inhibitory synapses, thus causing an excitation/inhibition imbalance in network excitability toward hyperexcitability that may be a determinant with regard to the development of epilepsy. Another approach to investigate epileptogenic mechanisms is to understand how silencing Syn affects the cellular behavior of single neurons and is associated with the hyperexcitable phenotypes observed in epilepsy. Here, we examined the functional effects of antisense-RNA inhibition of Syn expression on individually identified and isolated serotonergic cells of the Helix land snail. We found that Helix synapsin silencing increases cell excitability characterized by a slightly depolarized resting membrane potential, decreases the rheobase, reduces the threshold for action potential (AP) firing and increases the mean and instantaneous firing rates, with respect to control cells. The observed increase of Ca2+ and BK currents in Syn-silenced cells seems to be related to changes in the shape of the AP waveform. These currents sustain the faster spiking in Syn-deficient cells by increasing the after hyperpolarization and limiting the Na+ and Ca2+ channel inactivation during repetitive firing. This in turn speeds up the depolarization phase by reaching the AP threshold faster. Our results provide evidence that Syn silencing increases intrinsic cell excitability associated with increased Ca2+ and Ca2+-dependent BK currents in the absence of excitatory or inhibitory inputs.","lang":"eng"}],"type":"journal_article","date_published":"2015-12-17T00:00:00Z","publication":"Neuroscience","citation":{"chicago":"Brenes, Oscar, David H Vandael, Emilio Carbone, Pier Montarolo, and Mirella Ghirardi. “Knock-down of Synapsin Alters Cell Excitability and Action Potential Waveform by Potentiating BK and Voltage Gated Ca2 Currents in Helix Serotonergic Neurons.” Neuroscience. Elsevier, 2015. https://doi.org/10.1016/j.neuroscience.2015.10.046.","short":"O. Brenes, D.H. Vandael, E. Carbone, P. Montarolo, M. Ghirardi, Neuroscience 311 (2015) 430–443.","mla":"Brenes, Oscar, et al. “Knock-down of Synapsin Alters Cell Excitability and Action Potential Waveform by Potentiating BK and Voltage Gated Ca2 Currents in Helix Serotonergic Neurons.” Neuroscience, vol. 311, Elsevier, 2015, pp. 430–43, doi:10.1016/j.neuroscience.2015.10.046.","ieee":"O. Brenes, D. H. Vandael, E. Carbone, P. Montarolo, and M. Ghirardi, “Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons,” Neuroscience, vol. 311. Elsevier, pp. 430–443, 2015.","apa":"Brenes, O., Vandael, D. H., Carbone, E., Montarolo, P., & Ghirardi, M. (2015). Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. Elsevier. https://doi.org/10.1016/j.neuroscience.2015.10.046","ista":"Brenes O, Vandael DH, Carbone E, Montarolo P, Ghirardi M. 2015. Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. 311, 430–443.","ama":"Brenes O, Vandael DH, Carbone E, Montarolo P, Ghirardi M. Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons. Neuroscience. 2015;311:430-443. doi:10.1016/j.neuroscience.2015.10.046"},"article_type":"original","page":"430 - 443","day":"17","article_processing_charge":"No","has_accepted_license":"1","scopus_import":1,"author":[{"last_name":"Brenes","first_name":"Oscar","full_name":"Brenes, Oscar"},{"id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7577-1676","first_name":"David H","last_name":"Vandael","full_name":"Vandael, David H"},{"full_name":"Carbone, Emilio","last_name":"Carbone","first_name":"Emilio"},{"first_name":"Pier","last_name":"Montarolo","full_name":"Montarolo, Pier"},{"last_name":"Ghirardi","first_name":"Mirella","full_name":"Ghirardi, Mirella"}],"date_updated":"2021-01-12T06:51:44Z","date_created":"2018-12-11T11:52:50Z","volume":311,"year":"2015","publication_status":"published","department":[{"_id":"PeJo"}],"publisher":"Elsevier","file_date_updated":"2020-07-14T12:45:02Z","publist_id":"5591","doi":"10.1016/j.neuroscience.2015.10.046","language":[{"iso":"eng"}],"tmp":{"name":"Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode","short":"CC BY-NC-ND (4.0)","image":"/images/cc_by_nc_nd.png"},"oa":1,"quality_controlled":"1","month":"12"},{"status":"public","ddc":["570"],"title":"Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism","intvolume":" 13","_id":"1615","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file":[{"access_level":"open_access","file_name":"IST-2016-470-v1+1_1-s2.0-S2211124715010220-main.pdf","creator":"system","content_type":"application/pdf","file_size":2314406,"file_id":"5005","relation":"main_file","checksum":"44d30fbb543774b076b4938bd36af9d7","date_created":"2018-12-12T10:13:23Z","date_updated":"2020-07-14T12:45:07Z"}],"oa_version":"Published Version","pubrep_id":"470","type":"journal_article","abstract":[{"lang":"eng","text":"Loss-of-function mutations in the synaptic adhesion protein Neuroligin-4 are among the most common genetic abnormalities associated with autism spectrum disorders, but little is known about the function of Neuroligin-4 and the consequences of its loss. We assessed synaptic and network characteristics in Neuroligin-4 knockout mice, focusing on the hippocampus as a model brain region with a critical role in cognition and memory, and found that Neuroligin-4 deletion causes subtle defects of the protein composition and function of GABAergic synapses in the hippocampal CA3 region. Interestingly, these subtle synaptic changes are accompanied by pronounced perturbations of γ-oscillatory network activity, which has been implicated in cognitive function and is altered in multiple psychiatric and neurodevelopmental disorders. Our data provide important insights into the mechanisms by which Neuroligin-4-dependent GABAergic synapses may contribute to autism phenotypes and indicate new strategies for therapeutic approaches."}],"issue":"3","page":"516 - 523","publication":"Cell Reports","citation":{"apa":"Hammer, M., Krueger Burg, D., Tuffy, L., Cooper, B., Taschenberger, H., Goswami, S., … Brose, N. (2015). Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2015.09.011","ieee":"M. Hammer et al., “Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism,” Cell Reports, vol. 13, no. 3. Cell Press, pp. 516–523, 2015.","ista":"Hammer M, Krueger Burg D, Tuffy L, Cooper B, Taschenberger H, Goswami S, Ehrenreich H, Jonas PM, Varoqueaux F, Rhee J, Brose N. 2015. Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. 13(3), 516–523.","ama":"Hammer M, Krueger Burg D, Tuffy L, et al. Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism. Cell Reports. 2015;13(3):516-523. doi:10.1016/j.celrep.2015.09.011","chicago":"Hammer, Matthieu, Dilja Krueger Burg, Liam Tuffy, Benjamin Cooper, Holger Taschenberger, Sarit Goswami, Hannelore Ehrenreich, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.” Cell Reports. Cell Press, 2015. https://doi.org/10.1016/j.celrep.2015.09.011.","short":"M. Hammer, D. Krueger Burg, L. Tuffy, B. Cooper, H. Taschenberger, S. Goswami, H. Ehrenreich, P.M. Jonas, F. Varoqueaux, J. Rhee, N. Brose, Cell Reports 13 (2015) 516–523.","mla":"Hammer, Matthieu, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.” Cell Reports, vol. 13, no. 3, Cell Press, 2015, pp. 516–23, doi:10.1016/j.celrep.2015.09.011."},"date_published":"2015-10-20T00:00:00Z","scopus_import":1,"day":"20","has_accepted_license":"1","publication_status":"published","department":[{"_id":"PeJo"}],"publisher":"Cell Press","year":"2015","acknowledgement":"This work was supported by the Max Planck Society (N.B. and H.E.), the European Commission (EU-AIMS FP7-115300, N.B. and H.E.; Marie Curie IRG, D.K.-B.), the German Research Foundation (CNMPB, N.B., H.E., and F.V.), the Alexander von Humboldt-Foundation (D.K.-B.), and the Austrian Fond zur Förderung der Wissenschaftlichen Forschung (P 24909-B24, P.J.). M.H. was a student of the doctoral program Molecular Physiology of the Brain. Dr. J.-M. Fritschy generously provided the GABAARγ2 antibody. We thank F. Benseler, I. Thanhäuser, D. Schwerdtfeger, A. Ronnenberg, and D. Winkler for valuable advice and excellent technical support. We are grateful to the staff at the animal facility of the Max Planck Institute of Experimental Medicine for mouse husbandry.","date_updated":"2021-01-12T06:52:01Z","date_created":"2018-12-11T11:53:02Z","volume":13,"author":[{"last_name":"Hammer","first_name":"Matthieu","full_name":"Hammer, Matthieu"},{"last_name":"Krueger Burg","first_name":"Dilja","full_name":"Krueger Burg, Dilja"},{"full_name":"Tuffy, Liam","first_name":"Liam","last_name":"Tuffy"},{"first_name":"Benjamin","last_name":"Cooper","full_name":"Cooper, Benjamin"},{"full_name":"Taschenberger, Holger","last_name":"Taschenberger","first_name":"Holger"},{"full_name":"Goswami, Sarit","id":"3A578F32-F248-11E8-B48F-1D18A9856A87","first_name":"Sarit","last_name":"Goswami"},{"first_name":"Hannelore","last_name":"Ehrenreich","full_name":"Ehrenreich, Hannelore"},{"full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","first_name":"Peter M","last_name":"Jonas"},{"full_name":"Varoqueaux, Frederique","last_name":"Varoqueaux","first_name":"Frederique"},{"full_name":"Rhee, Jeong","first_name":"Jeong","last_name":"Rhee"},{"full_name":"Brose, Nils","last_name":"Brose","first_name":"Nils"}],"file_date_updated":"2020-07-14T12:45:07Z","publist_id":"5551","quality_controlled":"1","oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"language":[{"iso":"eng"}],"doi":"10.1016/j.celrep.2015.09.011","month":"10"},{"month":"01","project":[{"grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Mechanisms of transmitter release at GABAergic synapses"},{"_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","call_identifier":"FP7"}],"quality_controlled":"1","oa":1,"external_id":{"pmid":["25583495"]},"language":[{"iso":"eng"}],"doi":"10.1073/pnas.1412996112","ec_funded":1,"publist_id":"5552","file_date_updated":"2020-07-14T12:45:07Z","publisher":"National Academy of Sciences","department":[{"_id":"PeJo"}],"publication_status":"published","pmid":1,"year":"2015","volume":112,"date_created":"2018-12-11T11:53:02Z","date_updated":"2021-01-12T06:52:01Z","author":[{"first_name":"Michael","last_name":"Strüber","full_name":"Strüber, Michael"},{"first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"},{"full_name":"Bartos, Marlene","first_name":"Marlene","last_name":"Bartos"}],"scopus_import":1,"has_accepted_license":"1","day":"27","page":"1220 - 1225","citation":{"ista":"Strüber M, Jonas PM, Bartos M. 2015. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. 112(4), 1220–1225.","apa":"Strüber, M., Jonas, P. M., & Bartos, M. (2015). Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.1412996112","ieee":"M. Strüber, P. M. Jonas, and M. Bartos, “Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells,” PNAS, vol. 112, no. 4. National Academy of Sciences, pp. 1220–1225, 2015.","ama":"Strüber M, Jonas PM, Bartos M. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. 2015;112(4):1220-1225. doi:10.1073/pnas.1412996112","chicago":"Strüber, Michael, Peter M Jonas, and Marlene Bartos. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” PNAS. National Academy of Sciences, 2015. https://doi.org/10.1073/pnas.1412996112.","mla":"Strüber, Michael, et al. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” PNAS, vol. 112, no. 4, National Academy of Sciences, 2015, pp. 1220–25, doi:10.1073/pnas.1412996112.","short":"M. Strüber, P.M. Jonas, M. Bartos, PNAS 112 (2015) 1220–1225."},"publication":"PNAS","date_published":"2015-01-27T00:00:00Z","type":"journal_article","issue":"4","abstract":[{"text":"GABAergic perisoma-inhibiting fast-spiking interneurons (PIIs) effectively control the activity of large neuron populations by their wide axonal arborizations. It is generally assumed that the output of one PII to its target cells is strong and rapid. Here, we show that, unexpectedly, both strength and time course of PII-mediated perisomatic inhibition change with distance between synaptically connected partners in the rodent hippocampus. Synaptic signals become weaker due to lower contact numbers and decay more slowly with distance, very likely resulting from changes in GABAA receptor subunit composition. When distance-dependent synaptic inhibition is introduced to a rhythmically active neuronal network model, randomly driven principal cell assemblies are strongly synchronized by the PIIs, leading to higher precision in principal cell spike times than in a network with uniform synaptic inhibition. ","lang":"eng"}],"intvolume":" 112","title":"Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells","ddc":["570"],"status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1614","file":[{"checksum":"6703309a1f58493cf5a704211fb6ebed","date_updated":"2020-07-14T12:45:07Z","date_created":"2019-01-17T07:52:40Z","relation":"main_file","file_id":"5838","file_size":1280860,"content_type":"application/pdf","creator":"dernst","access_level":"open_access","file_name":"2015_PNAS_Strueber.pdf"}],"oa_version":"Published Version"},{"_id":"1845","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","title":"Excitement about inhibitory presynaptic terminals","ddc":["570"],"status":"public","intvolume":" 85","pubrep_id":"822","oa_version":"Published Version","file":[{"content_type":"application/pdf","file_size":411832,"creator":"system","access_level":"open_access","file_name":"IST-2017-822-v1+1_Perspective_Fig__Final.pdf","checksum":"d1808550e376a0eca2a950fda017cfa6","date_updated":"2020-07-14T12:45:19Z","date_created":"2018-12-12T10:16:07Z","relation":"main_file","file_id":"5192"},{"relation":"main_file","file_id":"5193","date_updated":"2020-07-14T12:45:19Z","date_created":"2018-12-12T10:16:07Z","checksum":"a279f4ae61e6c8f33d68f69a0d02097d","file_name":"IST-2017-822-v1+2_Perspective_Final2.pdf","access_level":"open_access","content_type":"application/pdf","file_size":100769,"creator":"system"}],"type":"journal_article","abstract":[{"text":"Based on extrapolation from excitatory synapses, it is often assumed that depletion of the releasable pool of synaptic vesicles is the main factor underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba (2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes in presynaptic action potential waveform substantially contribute to synaptic depression. Based on extrapolation from excitatory synapses, it is often assumed that depletion of the releasable pool of synaptic vesicles is the main factor underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba (2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes in presynaptic action potential waveform substantially contribute to synaptic depression.","lang":"eng"}],"issue":"6","publication":"Neuron","citation":{"short":"D.H. Vandael, C. Espinoza Martinez, P.M. Jonas, Neuron 85 (2015) 1149–1151.","mla":"Vandael, David H., et al. “Excitement about Inhibitory Presynaptic Terminals.” Neuron, vol. 85, no. 6, Elsevier, 2015, pp. 1149–51, doi:10.1016/j.neuron.2015.03.006.","chicago":"Vandael, David H, Claudia Espinoza Martinez, and Peter M Jonas. “Excitement about Inhibitory Presynaptic Terminals.” Neuron. Elsevier, 2015. https://doi.org/10.1016/j.neuron.2015.03.006.","ama":"Vandael DH, Espinoza Martinez C, Jonas PM. Excitement about inhibitory presynaptic terminals. Neuron. 2015;85(6):1149-1151. doi:10.1016/j.neuron.2015.03.006","apa":"Vandael, D. H., Espinoza Martinez, C., & Jonas, P. M. (2015). Excitement about inhibitory presynaptic terminals. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2015.03.006","ieee":"D. H. Vandael, C. Espinoza Martinez, and P. M. Jonas, “Excitement about inhibitory presynaptic terminals,” Neuron, vol. 85, no. 6. Elsevier, pp. 1149–1151, 2015.","ista":"Vandael DH, Espinoza Martinez C, Jonas PM. 2015. Excitement about inhibitory presynaptic terminals. Neuron. 85(6), 1149–1151."},"page":"1149 - 1151","date_published":"2015-03-18T00:00:00Z","scopus_import":"1","day":"18","has_accepted_license":"1","article_processing_charge":"No","year":"2015","publication_status":"published","publisher":"Elsevier","department":[{"_id":"PeJo"}],"author":[{"id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7577-1676","first_name":"David H","last_name":"Vandael","full_name":"Vandael, David H"},{"full_name":"Espinoza Martinez, Claudia ","last_name":"Espinoza Martinez","first_name":"Claudia ","orcid":"0000-0003-4710-2082","id":"31FFEE2E-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"date_created":"2018-12-11T11:54:19Z","date_updated":"2021-10-08T09:07:34Z","volume":85,"file_date_updated":"2020-07-14T12:45:19Z","publist_id":"5256","license":"https://creativecommons.org/licenses/by-nc/4.0/","tmp":{"name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","image":"/images/cc_by_nc.png","short":"CC BY-NC (4.0)"},"oa":1,"quality_controlled":"1","doi":"10.1016/j.neuron.2015.03.006","language":[{"iso":"eng"}],"month":"03"},{"oa_version":"Published Version","file":[{"date_updated":"2020-07-14T12:45:18Z","date_created":"2018-12-12T10:14:08Z","checksum":"53e16bd3fc2ae2c0d7de9164626c37aa","file_id":"5057","relation":"main_file","creator":"system","content_type":"application/pdf","file_size":1146814,"file_name":"IST-2016-456-v1+1_ASN_Neuro-2015-Chen-.pdf","access_level":"open_access"}],"pubrep_id":"456","intvolume":" 7","ddc":["570"],"title":"Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats","status":"public","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1834","issue":"2","abstract":[{"lang":"eng","text":"Huge body of evidences demonstrated that volatile anesthetics affect the hippocampal neurogenesis and neurocognitive functions, and most of them showed impairment at anesthetic dose. Here, we investigated the effect of low dose (1.8%) sevoflurane on hippocampal neurogenesis and dentate gyrus-dependent learning. Neonatal rats at postnatal day 4 to 6 (P4-6) were treated with 1.8% sevoflurane for 6 hours. Neurogenesis was quantified by bromodeoxyuridine labeling and electrophysiology recording. Four and seven weeks after treatment, the Morris water maze and contextual-fear discrimination learning tests were performed to determine the influence on spatial learning and pattern separation. A 6-hour treatment with 1.8% sevoflurane promoted hippocampal neurogenesis and increased the survival of newborn cells and the proportion of immature granular cells in the dentate gyrus of neonatal rats. Sevoflurane-treated rats performed better during the training days of the Morris water maze test and in contextual-fear discrimination learning test. These results suggest that a subanesthetic dose of sevoflurane promotes hippocampal neurogenesis in neonatal rats and facilitates their performance in dentate gyrus-dependent learning tasks."}],"type":"journal_article","date_published":"2015-04-13T00:00:00Z","article_type":"original","citation":{"ista":"Chen C, Wang C, Zhao X, Zhou T, Xu D, Wang Z, Wang Y. 2015. Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. 7(2).","apa":"Chen, C., Wang, C., Zhao, X., Zhou, T., Xu, D., Wang, Z., & Wang, Y. (2015). Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. SAGE Publications. https://doi.org/10.1177/1759091415575845","ieee":"C. Chen et al., “Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats,” ASN Neuro, vol. 7, no. 2. SAGE Publications, 2015.","ama":"Chen C, Wang C, Zhao X, et al. Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. 2015;7(2). doi:10.1177/1759091415575845","chicago":"Chen, Chong, Chao Wang, Xuan Zhao, Tao Zhou, Dao Xu, Zhi Wang, and Ying Wang. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” ASN Neuro. SAGE Publications, 2015. https://doi.org/10.1177/1759091415575845.","mla":"Chen, Chong, et al. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” ASN Neuro, vol. 7, no. 2, SAGE Publications, 2015, doi:10.1177/1759091415575845.","short":"C. Chen, C. Wang, X. Zhao, T. Zhou, D. Xu, Z. Wang, Y. Wang, ASN Neuro 7 (2015)."},"publication":"ASN Neuro","article_processing_charge":"No","has_accepted_license":"1","day":"13","scopus_import":"1","volume":7,"date_updated":"2023-10-18T06:47:30Z","date_created":"2018-12-11T11:54:16Z","author":[{"full_name":"Chen, Chong","first_name":"Chong","last_name":"Chen","id":"3DFD581A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Wang, Chao","first_name":"Chao","last_name":"Wang"},{"last_name":"Zhao","first_name":"Xuan","full_name":"Zhao, Xuan"},{"first_name":"Tao","last_name":"Zhou","full_name":"Zhou, Tao"},{"full_name":"Xu, Dao","last_name":"Xu","first_name":"Dao"},{"first_name":"Zhi","last_name":"Wang","full_name":"Wang, Zhi"},{"last_name":"Wang","first_name":"Ying","full_name":"Wang, Ying"}],"publisher":"SAGE Publications","department":[{"_id":"PeJo"}],"publication_status":"published","year":"2015","license":"https://creativecommons.org/licenses/by/3.0/","publist_id":"5269","file_date_updated":"2020-07-14T12:45:18Z","language":[{"iso":"eng"}],"doi":"10.1177/1759091415575845","quality_controlled":"1","tmp":{"legal_code_url":"https://creativecommons.org/licenses/by/3.0/legalcode","name":"Creative Commons Attribution 3.0 Unported (CC BY 3.0)","short":"CC BY (3.0)","image":"/images/cc_by.png"},"oa":1,"month":"04"},{"month":"02","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"language":[{"iso":"eng"}],"doi":"10.1111/psyp.12062","publist_id":"5205","file_date_updated":"2020-07-14T12:45:20Z","publisher":"Wiley-Blackwell","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"publication_status":"published","acknowledgement":"Funded by Austrian Science Fund (FWF) Grant Number: P 22189-B18; European Union within the 6th Framework Programme Grant Number: 517590; State government of Styria Grant Number: PN 4055","year":"2014","volume":51,"date_created":"2018-12-11T11:54:34Z","date_updated":"2021-01-12T06:53:52Z","author":[{"first_name":"Christof","last_name":"Körner","full_name":"Körner, Christof"},{"first_name":"Verena","last_name":"Braunstein","full_name":"Braunstein, Verena"},{"full_name":"Stangl, Matthias","first_name":"Matthias","last_name":"Stangl"},{"full_name":"Schlögl, Alois","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-5621-8100","first_name":"Alois","last_name":"Schlögl"},{"full_name":"Neuper, Christa","first_name":"Christa","last_name":"Neuper"},{"last_name":"Ischebeck","first_name":"Anja","full_name":"Ischebeck, Anja"}],"scopus_import":1,"has_accepted_license":"1","day":"11","page":"385 - 395","citation":{"ama":"Körner C, Braunstein V, Stangl M, Schlögl A, Neuper C, Ischebeck A. Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. Psychophysiology. 2014;51(4):385-395. doi:10.1111/psyp.12062","ieee":"C. Körner, V. Braunstein, M. Stangl, A. Schlögl, C. Neuper, and A. Ischebeck, “Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection,” Psychophysiology, vol. 51, no. 4. Wiley-Blackwell, pp. 385–395, 2014.","apa":"Körner, C., Braunstein, V., Stangl, M., Schlögl, A., Neuper, C., & Ischebeck, A. (2014). Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. Psychophysiology. Wiley-Blackwell. https://doi.org/10.1111/psyp.12062","ista":"Körner C, Braunstein V, Stangl M, Schlögl A, Neuper C, Ischebeck A. 2014. Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. Psychophysiology. 51(4), 385–395.","short":"C. Körner, V. Braunstein, M. Stangl, A. Schlögl, C. Neuper, A. Ischebeck, Psychophysiology 51 (2014) 385–395.","mla":"Körner, Christof, et al. “Sequential Effects in Continued Visual Search: Using Fixation-Related Potentials to Compare Distractor Processing before and after Target Detection.” Psychophysiology, vol. 51, no. 4, Wiley-Blackwell, 2014, pp. 385–95, doi:10.1111/psyp.12062.","chicago":"Körner, Christof, Verena Braunstein, Matthias Stangl, Alois Schlögl, Christa Neuper, and Anja Ischebeck. “Sequential Effects in Continued Visual Search: Using Fixation-Related Potentials to Compare Distractor Processing before and after Target Detection.” Psychophysiology. Wiley-Blackwell, 2014. https://doi.org/10.1111/psyp.12062."},"publication":"Psychophysiology","date_published":"2014-02-11T00:00:00Z","type":"journal_article","issue":"4","abstract":[{"lang":"eng","text":"To search for a target in a complex environment is an everyday behavior that ends with finding the target. When we search for two identical targets, however, we must continue the search after finding the first target and memorize its location. We used fixation-related potentials to investigate the neural correlates of different stages of the search, that is, before and after finding the first target. Having found the first target influenced subsequent distractor processing. Compared to distractor fixations before the first target fixation, a negative shift was observed for three subsequent distractor fixations. These results suggest that processing a target in continued search modulates the brain's response, either transiently by reflecting temporary working memory processes or permanently by reflecting working memory retention."}],"intvolume":" 51","status":"public","ddc":["000"],"title":"Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection","_id":"1890","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","oa_version":"Published Version","file":[{"access_level":"open_access","file_name":"IST-2016-442-v1+1_K-rner_et_al-2014-Psychophysiology.pdf","content_type":"application/pdf","file_size":543243,"creator":"system","relation":"main_file","file_id":"5233","checksum":"4255b6185e774acce1d99f8e195c564d","date_created":"2018-12-12T10:16:44Z","date_updated":"2020-07-14T12:45:20Z"}],"pubrep_id":"442"},{"date_published":"2014-11-19T00:00:00Z","citation":{"ista":"Kim S. 2014. Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. PLoS One. 9(11), 0113124.","apa":"Kim, S. (2014). Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0113124","ieee":"S. Kim, “Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus,” PLoS One, vol. 9, no. 11. Public Library of Science, 2014.","ama":"Kim S. Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. PLoS One. 2014;9(11). doi:10.1371/journal.pone.0113124","chicago":"Kim, Sooyun. “Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus.” PLoS One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0113124.","mla":"Kim, Sooyun. “Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus.” PLoS One, vol. 9, no. 11, 0113124, Public Library of Science, 2014, doi:10.1371/journal.pone.0113124.","short":"S. Kim, PLoS One 9 (2014)."},"publication":"PLoS One","has_accepted_license":"1","day":"19","scopus_import":1,"pubrep_id":"434","oa_version":"Published Version","file":[{"relation":"main_file","file_id":"5107","checksum":"85e4f4ea144f827272aaf376b2830564","date_created":"2018-12-12T10:14:52Z","date_updated":"2020-07-14T12:45:24Z","access_level":"open_access","file_name":"IST-2016-434-v1+1_journal.pone.0113124.pdf","file_size":5179993,"content_type":"application/pdf","creator":"system"}],"_id":"2002","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","intvolume":" 9","ddc":["570"],"status":"public","title":"Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus","issue":"11","abstract":[{"lang":"eng","text":"Oriens-lacunosum moleculare (O-LM) interneurons in the CA1 region of the hippocampus play a key role in feedback inhibition and in the control of network activity. However, how these cells are efficiently activated in the network remains unclear. To address this question, I performed recordings from CA1 pyramidal neuron axons, the presynaptic fibers that provide feedback innervation of these interneurons. Two forms of axonal action potential (AP) modulation were identified. First, repetitive stimulation resulted in activity-dependent AP broadening. Broadening showed fast onset, with marked changes in AP shape following a single AP. Second, tonic depolarization in CA1 pyramidal neuron somata induced AP broadening in the axon, and depolarization-induced broadening summated with activity-dependent broadening. Outsideout patch recordings from CA1 pyramidal neuron axons revealed a high density of a-dendrotoxin (α-DTX)-sensitive, inactivating K+ channels, suggesting that K+ channel inactivation mechanistically contributes to AP broadening. To examine the functional consequences of axonal AP modulation for synaptic transmission, I performed paired recordings between synaptically connected CA1 pyramidal neurons and O-LM interneurons. CA1 pyramidal neuron-O-LM interneuron excitatory postsynaptic currents (EPSCs) showed facilitation during both repetitive stimulation and tonic depolarization of the presynaptic neuron. Both effects were mimicked and occluded by α-DTX, suggesting that they were mediated by K+ channel inactivation. Therefore, axonal AP modulation can greatly facilitate the activation of O-LM interneurons. In conclusion, modulation of AP shape in CA1 pyramidal neuron axons substantially enhances the efficacy of principal neuron-interneuron synapses, promoting the activation of O-LM interneurons in recurrent inhibitory microcircuits."}],"type":"journal_article","doi":"10.1371/journal.pone.0113124","language":[{"iso":"eng"}],"oa":1,"tmp":{"short":"CC BY-SA (4.0)","image":"/images/cc_by_sa.png","name":"Creative Commons Attribution-ShareAlike 4.0 International Public License (CC BY-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-sa/4.0/legalcode"},"project":[{"call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548"}],"quality_controlled":"1","month":"11","author":[{"full_name":"Kim, Sooyun","first_name":"Sooyun","last_name":"Kim","id":"394AB1C8-F248-11E8-B48F-1D18A9856A87"}],"volume":9,"date_created":"2018-12-11T11:55:09Z","date_updated":"2021-01-12T06:54:39Z","year":"2014","publisher":"Public Library of Science","department":[{"_id":"PeJo"}],"publication_status":"published","publist_id":"5074","ec_funded":1,"file_date_updated":"2020-07-14T12:45:24Z","license":"https://creativecommons.org/licenses/by-sa/4.0/","article_number":"0113124"},{"oa_version":"Submitted Version","file":[{"creator":"system","file_size":2239563,"content_type":"application/pdf","access_level":"open_access","file_name":"IST-2016-421-v1+1_e04057.full.pdf","checksum":"c240f915450d4ebe8f95043a2a8c7b1a","date_updated":"2020-07-14T12:45:26Z","date_created":"2018-12-12T10:14:41Z","file_id":"5094","relation":"main_file"}],"pubrep_id":"421","title":"Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse","status":"public","ddc":["570"],"intvolume":" 3","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","_id":"2031","abstract":[{"text":"A puzzling property of synaptic transmission, originally established at the neuromuscular junction, is that the time course of transmitter release is independent of the extracellular Ca2+ concentration ([Ca2+]o), whereas the rate of release is highly [Ca2+]o-dependent. Here, we examine the time course of release at inhibitory basket cell-Purkinje cell synapses and show that it is independent of [Ca2+]o. Modeling of Ca2+-dependent transmitter release suggests that the invariant time course of release critically depends on tight coupling between Ca2+ channels and release sensors. Experiments with exogenous Ca2+ chelators reveal that channel-sensor coupling at basket cell-Purkinje cell synapses is very tight, with a mean distance of 10–20 nm. Thus, tight channel-sensor coupling provides a mechanistic explanation for the apparent [Ca2+]o independence of the time course of release.","lang":"eng"}],"type":"journal_article","date_published":"2014-12-09T00:00:00Z","publication":"eLife","citation":{"mla":"Arai, itaru, and Peter M. Jonas. “Nanodomain Coupling Explains Ca^2+ Independence of Transmitter Release Time Course at a Fast Central Synapse.” ELife, vol. 3, eLife Sciences Publications, 2014, doi:10.7554/eLife.04057.","short":"itaru Arai, P.M. Jonas, ELife 3 (2014).","chicago":"Arai, itaru, and Peter M Jonas. “Nanodomain Coupling Explains Ca^2+ Independence of Transmitter Release Time Course at a Fast Central Synapse.” ELife. eLife Sciences Publications, 2014. https://doi.org/10.7554/eLife.04057.","ama":"Arai itaru, Jonas PM. Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. eLife. 2014;3. doi:10.7554/eLife.04057","ista":"Arai itaru, Jonas PM. 2014. Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. eLife. 3.","ieee":"itaru Arai and P. M. Jonas, “Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse,” eLife, vol. 3. eLife Sciences Publications, 2014.","apa":"Arai, itaru, & Jonas, P. M. (2014). Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.04057"},"day":"09","has_accepted_license":"1","scopus_import":1,"date_created":"2018-12-11T11:55:19Z","date_updated":"2021-01-12T06:54:51Z","volume":3,"author":[{"id":"32A73F6C-F248-11E8-B48F-1D18A9856A87","first_name":"Itaru","last_name":"Arai","full_name":"Arai, Itaru"},{"full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804"}],"publication_status":"published","department":[{"_id":"PeJo"}],"publisher":"eLife Sciences Publications","year":"2014","file_date_updated":"2020-07-14T12:45:26Z","publist_id":"5041","ec_funded":1,"language":[{"iso":"eng"}],"doi":"10.7554/eLife.04057","quality_controlled":"1","project":[{"grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Mechanisms of transmitter release at GABAergic synapses"},{"_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548","call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"}],"oa":1,"month":"12"},{"type":"journal_article","abstract":[{"text":"The hippocampus mediates several higher brain functions, such as learning, memory, and spatial coding. The input region of the hippocampus, the dentate gyrus, plays a critical role in these processes. Several lines of evidence suggest that the dentate gyrus acts as a preprocessor of incoming information, preparing it for subsequent processing in CA3. For example, the dentate gyrus converts input from the entorhinal cortex, where cells have multiple spatial fields, into the spatially more specific place cell activity characteristic of the CA3 region. Furthermore, the dentate gyrus is involved in pattern separation, transforming relatively similar input patterns into substantially different output patterns. Finally, the dentate gyrus produces a very sparse coding scheme in which only a very small fraction of neurons are active at any one time.","lang":"eng"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","_id":"2041","intvolume":" 8","status":"public","title":"Structure, function and plasticity of hippocampal dentate gyrus microcircuits","ddc":["570"],"pubrep_id":"424","file":[{"relation":"main_file","file_id":"5294","checksum":"3ca57b164045523f876407e9f13a9fb8","date_updated":"2020-07-14T12:45:26Z","date_created":"2018-12-12T10:17:38Z","access_level":"open_access","file_name":"IST-2016-424-v1+1_fncir-08-00107.pdf","file_size":201110,"content_type":"application/pdf","creator":"system"}],"oa_version":"Published Version","scopus_import":1,"has_accepted_license":"1","day":"10","citation":{"ama":"Jonas PM, Lisman J. Structure, function and plasticity of hippocampal dentate gyrus microcircuits. Frontiers in Neural Circuits. 2014;8. doi:10.3389/fncir.2014.00107","apa":"Jonas, P. M., & Lisman, J. (2014). Structure, function and plasticity of hippocampal dentate gyrus microcircuits. Frontiers in Neural Circuits. Frontiers Research Foundation. https://doi.org/10.3389/fncir.2014.00107","ieee":"P. M. Jonas and J. Lisman, “Structure, function and plasticity of hippocampal dentate gyrus microcircuits,” Frontiers in Neural Circuits, vol. 8. Frontiers Research Foundation, 2014.","ista":"Jonas PM, Lisman J. 2014. Structure, function and plasticity of hippocampal dentate gyrus microcircuits. Frontiers in Neural Circuits. 8, 2p.","short":"P.M. Jonas, J. Lisman, Frontiers in Neural Circuits 8 (2014).","mla":"Jonas, Peter M., and John Lisman. “Structure, Function and Plasticity of Hippocampal Dentate Gyrus Microcircuits.” Frontiers in Neural Circuits, vol. 8, 2p, Frontiers Research Foundation, 2014, doi:10.3389/fncir.2014.00107.","chicago":"Jonas, Peter M, and John Lisman. “Structure, Function and Plasticity of Hippocampal Dentate Gyrus Microcircuits.” Frontiers in Neural Circuits. Frontiers Research Foundation, 2014. https://doi.org/10.3389/fncir.2014.00107."},"publication":"Frontiers in Neural Circuits","date_published":"2014-09-10T00:00:00Z","article_number":"2p","publist_id":"5010","file_date_updated":"2020-07-14T12:45:26Z","year":"2014","publisher":"Frontiers Research Foundation","department":[{"_id":"PeJo"}],"publication_status":"published","author":[{"full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","first_name":"Peter M","last_name":"Jonas"},{"full_name":"Lisman, John","first_name":"John","last_name":"Lisman"}],"volume":8,"date_updated":"2021-01-12T06:54:55Z","date_created":"2018-12-11T11:55:22Z","month":"09","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"quality_controlled":"1","doi":"10.3389/fncir.2014.00107","language":[{"iso":"eng"}]},{"citation":{"ama":"Hu H, Gan J, Jonas PM. Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. Science. 2014;345(6196). doi:10.1126/science.1255263","ieee":"H. Hu, J. Gan, and P. M. Jonas, “Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function,” Science, vol. 345, no. 6196. American Association for the Advancement of Science, 2014.","apa":"Hu, H., Gan, J., & Jonas, P. M. (2014). Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1255263","ista":"Hu H, Gan J, Jonas PM. 2014. Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. Science. 345(6196), 1255263.","short":"H. Hu, J. Gan, P.M. Jonas, Science 345 (2014).","mla":"Hu, Hua, et al. “Fast-Spiking Parvalbumin^+ GABAergic Interneurons: From Cellular Design to Microcircuit Function.” Science, vol. 345, no. 6196, 1255263, American Association for the Advancement of Science, 2014, doi:10.1126/science.1255263.","chicago":"Hu, Hua, Jian Gan, and Peter M Jonas. “Fast-Spiking Parvalbumin^+ GABAergic Interneurons: From Cellular Design to Microcircuit Function.” Science. American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1255263."},"publication":"Science","date_published":"2014-08-01T00:00:00Z","scopus_import":1,"has_accepted_license":"1","day":"01","_id":"2062","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","intvolume":" 345","status":"public","ddc":["570"],"title":"Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function","pubrep_id":"821","oa_version":"Submitted Version","file":[{"relation":"main_file","file_id":"5185","checksum":"a0036a589037d37e86364fa25cc0a82f","date_updated":"2020-07-14T12:45:27Z","date_created":"2018-12-12T10:16:00Z","access_level":"open_access","file_name":"IST-2017-821-v1+1_1255263JonasPVReviewTextR_Final.pdf","content_type":"application/pdf","file_size":215514,"creator":"system"},{"file_size":1732723,"content_type":"application/pdf","creator":"system","access_level":"open_access","file_name":"IST-2017-821-v1+2_1255263JonasPVReviewFigures_Final.pdf","checksum":"e1f57d2713725449cb898fdcb8ef47b8","date_updated":"2020-07-14T12:45:27Z","date_created":"2018-12-12T10:16:01Z","relation":"main_file","file_id":"5186"}],"type":"journal_article","issue":"6196","abstract":[{"lang":"eng","text":"The success story of fast-spiking, parvalbumin-positive (PV+) GABAergic interneurons (GABA, γ-aminobutyric acid) in the mammalian central nervous system is noteworthy. In 1995, the properties of these interneurons were completely unknown. Twenty years later, thanks to the massive use of subcellular patch-clamp techniques, simultaneous multiple-cell recording, optogenetics, in vivo measurements, and computational approaches, our knowledge about PV+ interneurons became more extensive than for several types of pyramidal neurons. These findings have implications beyond the “small world” of basic research on GABAergic cells. For example, the results provide a first proof of principle that neuroscientists might be able to close the gaps between the molecular, cellular, network, and behavioral levels, representing one of the main challenges at the present time. Furthermore, the results may form the basis for PV+ interneurons as therapeutic targets for brain disease in the future. However, much needs to be learned about the basic function of these interneurons before clinical neuroscientists will be able to use PV+ interneurons for therapeutic purposes."}],"oa":1,"project":[{"name":"Mechanisms of transmitter release at GABAergic synapses","call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","grant_number":"P24909-B24"},{"name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","call_identifier":"FP7","_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548"}],"quality_controlled":"1","doi":"10.1126/science.1255263","language":[{"iso":"eng"}],"month":"08","year":"2014","publisher":"American Association for the Advancement of Science","department":[{"_id":"PeJo"}],"publication_status":"published","author":[{"last_name":"Hu","first_name":"Hua","id":"4AC0145C-F248-11E8-B48F-1D18A9856A87","full_name":"Hu, Hua"},{"first_name":"Jian","last_name":"Gan","id":"3614E438-F248-11E8-B48F-1D18A9856A87","full_name":"Gan, Jian"},{"last_name":"Jonas","first_name":"Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M"}],"volume":345,"date_created":"2018-12-11T11:55:29Z","date_updated":"2021-01-12T06:55:03Z","article_number":"1255263","ec_funded":1,"publist_id":"4984","file_date_updated":"2020-07-14T12:45:27Z"},{"volume":24,"oa_version":"None","date_created":"2018-12-11T11:56:04Z","date_updated":"2021-01-12T06:55:43Z","author":[{"last_name":"Chai","first_name":"Xuejun","full_name":"Chai, Xuejun"},{"last_name":"Münzner","first_name":"Gert","full_name":"Münzner, Gert"},{"first_name":"Shanting","last_name":"Zhao","full_name":"Zhao, Shanting"},{"last_name":"Tinnes","first_name":"Stefanie","full_name":"Tinnes, Stefanie"},{"full_name":"Kowalski, Janina","id":"3F3CA136-F248-11E8-B48F-1D18A9856A87","first_name":"Janina","last_name":"Kowalski"},{"full_name":"Häussler, Ute","last_name":"Häussler","first_name":"Ute"},{"full_name":"Young, Christina","last_name":"Young","first_name":"Christina"},{"last_name":"Haas","first_name":"Carola","full_name":"Haas, Carola"},{"full_name":"Frotscher, Michael","first_name":"Michael","last_name":"Frotscher"}],"intvolume":" 24","department":[{"_id":"PeJo"}],"publisher":"Oxford University Press","title":"Epilepsy-induced motility of differentiated neurons","publication_status":"published","status":"public","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","_id":"2164","year":"2014","issue":"8","publist_id":"4820","abstract":[{"lang":"eng","text":"Neuronal ectopia, such as granule cell dispersion (GCD) in temporal lobe epilepsy (TLE), has been assumed to result from a migration defect during development. Indeed, recent studies reported that aberrant migration of neonatal-generated dentate granule cells (GCs) increased the risk to develop epilepsy later in life. On the contrary, in the present study, we show that fully differentiated GCs become motile following the induction of epileptiform activity, resulting in GCD. Hippocampal slice cultures from transgenic mice expressing green fluorescent protein in differentiated, but not in newly generated GCs, were incubated with the glutamate receptor agonist kainate (KA), which induced GC burst activity and GCD. Using real-time microscopy, we observed that KA-exposed, differentiated GCs translocated their cell bodies and changed their dendritic organization. As found in human TLE, KA application was associated with decreased expression of the extracellular matrix protein Reelin, particularly in hilar interneurons. Together these findings suggest that KA-induced motility of differentiated GCs contributes to the development of GCD and establish slice cultures as a model to study neuronal changes induced by epileptiform activity. "}],"type":"journal_article","language":[{"iso":"eng"}],"doi":"10.1093/cercor/bht067","date_published":"2014-08-01T00:00:00Z","page":"2130 - 2140","quality_controlled":"1","citation":{"mla":"Chai, Xuejun, et al. “Epilepsy-Induced Motility of Differentiated Neurons.” Cerebral Cortex, vol. 24, no. 8, Oxford University Press, 2014, pp. 2130–40, doi:10.1093/cercor/bht067.","short":"X. Chai, G. Münzner, S. Zhao, S. Tinnes, J. Kowalski, U. Häussler, C. Young, C. Haas, M. Frotscher, Cerebral Cortex 24 (2014) 2130–2140.","chicago":"Chai, Xuejun, Gert Münzner, Shanting Zhao, Stefanie Tinnes, Janina Kowalski, Ute Häussler, Christina Young, Carola Haas, and Michael Frotscher. “Epilepsy-Induced Motility of Differentiated Neurons.” Cerebral Cortex. Oxford University Press, 2014. https://doi.org/10.1093/cercor/bht067.","ama":"Chai X, Münzner G, Zhao S, et al. Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. 2014;24(8):2130-2140. doi:10.1093/cercor/bht067","ista":"Chai X, Münzner G, Zhao S, Tinnes S, Kowalski J, Häussler U, Young C, Haas C, Frotscher M. 2014. Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. 24(8), 2130–2140.","ieee":"X. Chai et al., “Epilepsy-induced motility of differentiated neurons,” Cerebral Cortex, vol. 24, no. 8. Oxford University Press, pp. 2130–2140, 2014.","apa":"Chai, X., Münzner, G., Zhao, S., Tinnes, S., Kowalski, J., Häussler, U., … Frotscher, M. (2014). Epilepsy-induced motility of differentiated neurons. Cerebral Cortex. Oxford University Press. https://doi.org/10.1093/cercor/bht067"},"publication":"Cerebral Cortex","day":"01","month":"08","scopus_import":1},{"month":"05","day":"29","scopus_import":1,"date_published":"2014-05-29T00:00:00Z","doi":"10.1038/nprot.2014.099","language":[{"iso":"eng"}],"citation":{"short":"D. Studer, S. Zhao, X. Chai, P.M. Jonas, W. Graber, S. Nestel, M. Frotscher, Nature Protocols 9 (2014) 1480–1495.","mla":"Studer, Daniel, et al. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” Nature Protocols, vol. 9, no. 6, Nature Publishing Group, 2014, pp. 1480–95, doi:10.1038/nprot.2014.099.","chicago":"Studer, Daniel, Shanting Zhao, Xuejun Chai, Peter M Jonas, Werner Graber, Sigrun Nestel, and Michael Frotscher. “Capture of Activity-Induced Ultrastructural Changes at Synapses by High-Pressure Freezing of Brain Tissue.” Nature Protocols. Nature Publishing Group, 2014. https://doi.org/10.1038/nprot.2014.099.","ama":"Studer D, Zhao S, Chai X, et al. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. 2014;9(6):1480-1495. doi:10.1038/nprot.2014.099","ieee":"D. Studer et al., “Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue,” Nature Protocols, vol. 9, no. 6. Nature Publishing Group, pp. 1480–1495, 2014.","apa":"Studer, D., Zhao, S., Chai, X., Jonas, P. M., Graber, W., Nestel, S., & Frotscher, M. (2014). Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. Nature Publishing Group. https://doi.org/10.1038/nprot.2014.099","ista":"Studer D, Zhao S, Chai X, Jonas PM, Graber W, Nestel S, Frotscher M. 2014. Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue. Nature Protocols. 9(6), 1480–1495."},"publication":"Nature Protocols","project":[{"name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","_id":"25BDE9A4-B435-11E9-9278-68D0E5697425","grant_number":"SFB-TR3-TP10B"}],"page":"1480 - 1495","quality_controlled":"1","publist_id":"4807","issue":"6","abstract":[{"text":"Electron microscopy (EM) allows for the simultaneous visualization of all tissue components at high resolution. However, the extent to which conventional aldehyde fixation and ethanol dehydration of the tissue alter the fine structure of cells and organelles, thereby preventing detection of subtle structural changes induced by an experiment, has remained an issue. Attempts have been made to rapidly freeze tissue to preserve native ultrastructure. Shock-freezing of living tissue under high pressure (high-pressure freezing, HPF) followed by cryosubstitution of the tissue water avoids aldehyde fixation and dehydration in ethanol; the tissue water is immobilized in â ̂1/450 ms, and a close-to-native fine structure of cells, organelles and molecules is preserved. Here we describe a protocol for HPF that is useful to monitor ultrastructural changes associated with functional changes at synapses in the brain but can be applied to many other tissues as well. The procedure requires a high-pressure freezer and takes a minimum of 7 d but can be paused at several points.","lang":"eng"}],"type":"journal_article","author":[{"first_name":"Daniel","last_name":"Studer","full_name":"Studer, Daniel"},{"last_name":"Zhao","first_name":"Shanting","full_name":"Zhao, Shanting"},{"full_name":"Chai, Xuejun","last_name":"Chai","first_name":"Xuejun"},{"full_name":"Jonas, Peter M","last_name":"Jonas","first_name":"Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Graber, Werner","first_name":"Werner","last_name":"Graber"},{"last_name":"Nestel","first_name":"Sigrun","full_name":"Nestel, Sigrun"},{"first_name":"Michael","last_name":"Frotscher","full_name":"Frotscher, Michael"}],"volume":9,"oa_version":"None","date_updated":"2021-01-12T06:55:47Z","date_created":"2018-12-11T11:56:09Z","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","_id":"2176","year":"2014","intvolume":" 9","department":[{"_id":"PeJo"}],"publisher":"Nature Publishing Group","publication_status":"published","title":"Capture of activity-induced ultrastructural changes at synapses by high-pressure freezing of brain tissue","status":"public"},{"scopus_import":1,"day":"21","has_accepted_license":"1","publication":"Frontiers in Neuroinformatics","citation":{"short":"J. Guzmán, A. Schlögl, C. Schmidt Hieber, Frontiers in Neuroinformatics 8 (2014).","mla":"Guzmán, José, et al. “Stimfit: Quantifying Electrophysiological Data with Python.” Frontiers in Neuroinformatics, vol. 8, no. FEB, 16, Frontiers Research Foundation, 2014, doi:10.3389/fninf.2014.00016.","chicago":"Guzmán, José, Alois Schlögl, and Christoph Schmidt Hieber. “Stimfit: Quantifying Electrophysiological Data with Python.” Frontiers in Neuroinformatics. Frontiers Research Foundation, 2014. https://doi.org/10.3389/fninf.2014.00016.","ama":"Guzmán J, Schlögl A, Schmidt Hieber C. Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. 2014;8(FEB). doi:10.3389/fninf.2014.00016","ieee":"J. Guzmán, A. Schlögl, and C. Schmidt Hieber, “Stimfit: Quantifying electrophysiological data with Python,” Frontiers in Neuroinformatics, vol. 8, no. FEB. Frontiers Research Foundation, 2014.","apa":"Guzmán, J., Schlögl, A., & Schmidt Hieber, C. (2014). Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. Frontiers Research Foundation. https://doi.org/10.3389/fninf.2014.00016","ista":"Guzmán J, Schlögl A, Schmidt Hieber C. 2014. Stimfit: Quantifying electrophysiological data with Python. Frontiers in Neuroinformatics. 8(FEB), 16."},"date_published":"2014-02-21T00:00:00Z","type":"journal_article","abstract":[{"lang":"eng","text":"Intracellular electrophysiological recordings provide crucial insights into elementary neuronal signals such as action potentials and synaptic currents. Analyzing and interpreting these signals is essential for a quantitative understanding of neuronal information processing, and requires both fast data visualization and ready access to complex analysis routines. To achieve this goal, we have developed Stimfit, a free software package for cellular neurophysiology with a Python scripting interface and a built-in Python shell. The program supports most standard file formats for cellular neurophysiology and other biomedical signals through the Biosig library. To quantify and interpret the activity of single neurons and communication between neurons, the program includes algorithms to characterize the kinetics of presynaptic action potentials and postsynaptic currents, estimate latencies between pre- and postsynaptic events, and detect spontaneously occurring events. We validate and benchmark these algorithms, give estimation errors, and provide sample use cases, showing that Stimfit represents an efficient, accessible and extensible way to accurately analyze and interpret neuronal signals."}],"issue":"FEB","status":"public","title":"Stimfit: Quantifying electrophysiological data with Python","ddc":["570"],"intvolume":" 8","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"2230","file":[{"access_level":"open_access","file_name":"IST-2016-425-v1+1_fninf-08-00016.pdf","creator":"system","file_size":2883372,"content_type":"application/pdf","file_id":"4935","relation":"main_file","checksum":"eeca00bba7232ff7d27db83321f6ea30","date_created":"2018-12-12T10:12:17Z","date_updated":"2020-07-14T12:45:34Z"}],"oa_version":"Published Version","pubrep_id":"425","month":"02","publication_identifier":{"issn":["16625196"]},"quality_controlled":"1","tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"language":[{"iso":"eng"}],"doi":"10.3389/fninf.2014.00016","article_number":"16","file_date_updated":"2020-07-14T12:45:34Z","publist_id":"4731","publication_status":"published","publisher":"Frontiers Research Foundation","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"year":"2014","date_created":"2018-12-11T11:56:27Z","date_updated":"2021-01-12T06:56:09Z","volume":8,"author":[{"first_name":"José","last_name":"Guzmán","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","full_name":"Guzmán, José"},{"id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-5621-8100","first_name":"Alois","last_name":"Schlögl","full_name":"Schlögl, Alois"},{"full_name":"Schmidt Hieber, Christoph","first_name":"Christoph","last_name":"Schmidt Hieber"}]},{"ec_funded":1,"publist_id":"4733","author":[{"full_name":"Hu, Hua","id":"4AC0145C-F248-11E8-B48F-1D18A9856A87","last_name":"Hu","first_name":"Hua"},{"first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"volume":17,"date_created":"2018-12-11T11:56:26Z","date_updated":"2021-01-12T06:56:08Z","year":"2014","publisher":"Nature Publishing Group","department":[{"_id":"PeJo"}],"publication_status":"published","publication_identifier":{"issn":["10976256"]},"month":"03","doi":"10.1038/nn.3678","language":[{"iso":"eng"}],"oa":1,"main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4286295/","open_access":"1"}],"project":[{"call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","grant_number":"268548","_id":"25C0F108-B435-11E9-9278-68D0E5697425"},{"call_identifier":"FWF","name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"}],"quality_controlled":"1","issue":"5","abstract":[{"text":"Fast-spiking, parvalbumin-expressing GABAergic interneurons, a large proportion of which are basket cells (BCs), have a key role in feedforward and feedback inhibition, gamma oscillations and complex information processing. For these functions, fast propagation of action potentials (APs) from the soma to the presynaptic terminals is important. However, the functional properties of interneuron axons remain elusive. We examined interneuron axons by confocally targeted subcellular patch-clamp recording in rat hippocampal slices. APs were initiated in the proximal axon ∼20 μm from the soma and propagated to the distal axon with high reliability and speed. Subcellular mapping revealed a stepwise increase of Na^+ conductance density from the soma to the proximal axon, followed by a further gradual increase in the distal axon. Active cable modeling and experiments with partial channel block revealed that low axonal Na^+ conductance density was sufficient for reliability, but high Na^+ density was necessary for both speed of propagation and fast-spiking AP phenotype. Our results suggest that a supercritical density of Na^+ channels compensates for the morphological properties of interneuron axons (small segmental diameter, extensive branching and high bouton density), ensuring fast AP propagation and high-frequency repetitive firing.","lang":"eng"}],"type":"journal_article","oa_version":"Submitted Version","_id":"2228","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","intvolume":" 17","status":"public","title":"A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons","day":"23","scopus_import":1,"date_published":"2014-03-23T00:00:00Z","citation":{"ieee":"H. Hu and P. M. Jonas, “A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons,” Nature Neuroscience, vol. 17, no. 5. Nature Publishing Group, pp. 686–693, 2014.","apa":"Hu, H., & Jonas, P. M. (2014). A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3678","ista":"Hu H, Jonas PM. 2014. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. 17(5), 686–693.","ama":"Hu H, Jonas PM. A supercritical density of Na^+ channels ensures fast signaling in GABAergic interneuron axons. Nature Neuroscience. 2014;17(5):686-693. doi:10.1038/nn.3678","chicago":"Hu, Hua, and Peter M Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” Nature Neuroscience. Nature Publishing Group, 2014. https://doi.org/10.1038/nn.3678.","short":"H. Hu, P.M. Jonas, Nature Neuroscience 17 (2014) 686–693.","mla":"Hu, Hua, and Peter M. Jonas. “A Supercritical Density of Na^+ Channels Ensures Fast Signaling in GABAergic Interneuron Axons.” Nature Neuroscience, vol. 17, no. 5, Nature Publishing Group, 2014, pp. 686–93, doi:10.1038/nn.3678."},"publication":"Nature Neuroscience","page":"686-693"},{"main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617475/"}],"oa":1,"project":[{"name":"Mechanisms of transmitter release at GABAergic synapses","call_identifier":"FWF","grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"},{"grant_number":"268548","_id":"25C0F108-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"}],"quality_controlled":"1","doi":"10.1126/science.1244811","language":[{"iso":"eng"}],"publication_identifier":{"issn":["00368075"]},"month":"02","year":"2014","department":[{"_id":"PeJo"}],"publisher":"American Association for the Advancement of Science","publication_status":"published","author":[{"id":"36C4978E-F248-11E8-B48F-1D18A9856A87","last_name":"Vyleta","first_name":"Nicholas","full_name":"Vyleta, Nicholas"},{"first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"volume":343,"date_updated":"2021-01-12T06:56:09Z","date_created":"2018-12-11T11:56:27Z","ec_funded":1,"publist_id":"4732","citation":{"ieee":"N. Vyleta and P. M. Jonas, “Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse,” Science, vol. 343, no. 6171. American Association for the Advancement of Science, pp. 665–670, 2014.","apa":"Vyleta, N., & Jonas, P. M. (2014). Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1244811","ista":"Vyleta N, Jonas PM. 2014. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. 343(6171), 665–670.","ama":"Vyleta N, Jonas PM. Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse. Science. 2014;343(6171):665-670. doi:10.1126/science.1244811","chicago":"Vyleta, Nicholas, and Peter M Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” Science. American Association for the Advancement of Science, 2014. https://doi.org/10.1126/science.1244811.","short":"N. Vyleta, P.M. Jonas, Science 343 (2014) 665–670.","mla":"Vyleta, Nicholas, and Peter M. Jonas. “Loose Coupling between Ca^2+ Channels and Release Sensors at a Plastic Hippocampal Synapse.” Science, vol. 343, no. 6171, American Association for the Advancement of Science, 2014, pp. 665–70, doi:10.1126/science.1244811."},"publication":"Science","page":"665 - 670","date_published":"2014-02-01T00:00:00Z","scopus_import":1,"day":"01","_id":"2229","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","intvolume":" 343","title":"Loose coupling between Ca^2+ channels and release sensors at a plastic hippocampal synapse","status":"public","oa_version":"Submitted Version","type":"journal_article","issue":"6171","abstract":[{"lang":"eng","text":"The distance between Ca^2+ channels and release sensors determines the speed and efficacy of synaptic transmission. Tight "nanodomain" channel-sensor coupling initiates transmitter release at synapses in the mature brain, whereas loose "microdomain" coupling appears restricted to early developmental stages. To probe the coupling configuration at a plastic synapse in the mature central nervous system, we performed paired recordings between mossy fiber terminals and CA3 pyramidal neurons in rat hippocampus. Millimolar concentrations of both the fast Ca^2+ chelator BAPTA [1,2-bis(2-aminophenoxy)ethane- N,N, N′,N′-tetraacetic acid] and the slow chelator EGTA efficiently suppressed transmitter release, indicating loose coupling between Ca^2+ channels and release sensors. Loose coupling enabled the control of initial release probability by fast endogenous Ca^2+ buffers and the generation of facilitation by buffer saturation. Thus, loose coupling provides the molecular framework for presynaptic plasticity."}]},{"ec_funded":1,"publist_id":"4692","file_date_updated":"2020-07-14T12:45:35Z","year":"2014","publisher":"Elsevier","department":[{"_id":"PeJo"}],"publication_status":"published","author":[{"full_name":"Pernia-Andrade, Alejandro","first_name":"Alejandro","last_name":"Pernia-Andrade","id":"36963E98-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","first_name":"Peter M","full_name":"Jonas, Peter M"}],"volume":81,"date_updated":"2021-01-12T06:56:19Z","date_created":"2018-12-11T11:56:35Z","publication_identifier":{"issn":["08966273"]},"month":"01","oa":1,"project":[{"_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548","call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"},{"grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","name":"Mechanisms of transmitter release at GABAergic synapses"}],"quality_controlled":"1","doi":"10.1016/j.neuron.2013.09.046","language":[{"iso":"eng"}],"type":"journal_article","issue":"1","abstract":[{"text":"Theta-gamma network oscillations are thought to represent key reference signals for information processing in neuronal ensembles, but the underlying synaptic mechanisms remain unclear. To address this question, we performed whole-cell (WC) patch-clamp recordings from mature hippocampal granule cells (GCs) in vivo in the dentate gyrus of anesthetized and awake rats. GCs in vivo fired action potentials at low frequency, consistent with sparse coding in the dentate gyrus. GCs were exposed to barrages of fast AMPAR-mediated excitatory postsynaptic currents (EPSCs), primarily relayed from the entorhinal cortex, and inhibitory postsynaptic currents (IPSCs), presumably generated by local interneurons. EPSCs exhibited coherence with the field potential predominantly in the theta frequency band, whereas IPSCs showed coherence primarily in the gamma range. Action potentials in GCs were phase locked to network oscillations. Thus, theta-gamma-modulated synaptic currents may provide a framework for sparse temporal coding of information in the dentate gyrus.","lang":"eng"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"2254","intvolume":" 81","ddc":["570"],"title":"Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations","status":"public","pubrep_id":"422","file":[{"file_size":4373072,"content_type":"application/pdf","creator":"system","file_name":"IST-2016-422-v1+1_1-s2.0-S0896627313009227-main.pdf","access_level":"open_access","date_created":"2018-12-12T10:09:48Z","date_updated":"2020-07-14T12:45:35Z","checksum":"438547cfcd9045a22f065f2019f07849","relation":"main_file","file_id":"4773"}],"oa_version":"Published Version","scopus_import":1,"has_accepted_license":"1","day":"08","citation":{"mla":"Pernia-Andrade, Alejandro, and Peter M. Jonas. “Theta-Gamma-Modulated Synaptic Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.” Neuron, vol. 81, no. 1, Elsevier, 2014, pp. 140–52, doi:10.1016/j.neuron.2013.09.046.","short":"A. Pernia-Andrade, P.M. Jonas, Neuron 81 (2014) 140–152.","chicago":"Pernia-Andrade, Alejandro, and Peter M Jonas. “Theta-Gamma-Modulated Synaptic Currents in Hippocampal Granule Cells in Vivo Define a Mechanism for Network Oscillations.” Neuron. Elsevier, 2014. https://doi.org/10.1016/j.neuron.2013.09.046.","ama":"Pernia-Andrade A, Jonas PM. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. 2014;81(1):140-152. doi:10.1016/j.neuron.2013.09.046","ista":"Pernia-Andrade A, Jonas PM. 2014. Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. 81(1), 140–152.","apa":"Pernia-Andrade, A., & Jonas, P. M. (2014). Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2013.09.046","ieee":"A. Pernia-Andrade and P. M. Jonas, “Theta-gamma-modulated synaptic currents in hippocampal granule cells in vivo define a mechanism for network oscillations,” Neuron, vol. 81, no. 1. Elsevier, pp. 140–152, 2014."},"publication":"Neuron","page":"140 - 152","date_published":"2014-01-08T00:00:00Z"},{"month":"02","quality_controlled":"1","oa":1,"tmp":{"name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","image":"/images/cc_by_nc.png","short":"CC BY-NC (4.0)"},"language":[{"iso":"eng"}],"doi":"10.1002/hipo.22214","publist_id":"4646","file_date_updated":"2020-07-14T12:45:37Z","department":[{"_id":"PeJo"}],"publisher":"Wiley-Blackwell","publication_status":"published","year":"2014","acknowledgement":"Funded by Deutsche Forschungsgemeinschaft. Grant Numbers: SFB 505, SFB 780, BA1582/2-1 Excellence Initiative of the German Research Foundation (Spemann Graduate School). Grant Number: GSC-4 Lichtenberg Professorship-Award (VW-Foundation); Schram-Foundation; Excellence Initiative Brain Links-Brain Tools. The authors thank Drs. Jonas-Frederic Sauer and Claudio Elgueta for critically reading the manuscript. They also thank Karin Winterhalter, Margit Northemann and Ulrich Nöller for technical assistance.","volume":23,"date_updated":"2021-01-12T06:56:32Z","date_created":"2018-12-11T11:56:46Z","author":[{"full_name":"Hosp, Jonas","first_name":"Jonas","last_name":"Hosp"},{"last_name":"Strüber","first_name":"Michael","full_name":"Strüber, Michael"},{"first_name":"Yuchio","last_name":"Yanagawa","full_name":"Yanagawa, Yuchio"},{"full_name":"Obata, Kunihiko","first_name":"Kunihiko","last_name":"Obata"},{"last_name":"Vida","first_name":"Imre","full_name":"Vida, Imre"},{"full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","first_name":"Peter M","last_name":"Jonas"},{"first_name":"Marlene","last_name":"Bartos","full_name":"Bartos, Marlene"}],"scopus_import":1,"has_accepted_license":"1","day":"01","page":"189 - 203","citation":{"chicago":"Hosp, Jonas, Michael Strüber, Yuchio Yanagawa, Kunihiko Obata, Imre Vida, Peter M Jonas, and Marlene Bartos. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons into Classes.” Hippocampus. Wiley-Blackwell, 2014. https://doi.org/10.1002/hipo.22214.","short":"J. Hosp, M. Strüber, Y. Yanagawa, K. Obata, I. Vida, P.M. Jonas, M. Bartos, Hippocampus 23 (2014) 189–203.","mla":"Hosp, Jonas, et al. “Morpho-Physiological Criteria Divide Dentate Gyrus Interneurons into Classes.” Hippocampus, vol. 23, no. 2, Wiley-Blackwell, 2014, pp. 189–203, doi:10.1002/hipo.22214.","apa":"Hosp, J., Strüber, M., Yanagawa, Y., Obata, K., Vida, I., Jonas, P. M., & Bartos, M. (2014). Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. Wiley-Blackwell. https://doi.org/10.1002/hipo.22214","ieee":"J. Hosp et al., “Morpho-physiological criteria divide dentate gyrus interneurons into classes,” Hippocampus, vol. 23, no. 2. Wiley-Blackwell, pp. 189–203, 2014.","ista":"Hosp J, Strüber M, Yanagawa Y, Obata K, Vida I, Jonas PM, Bartos M. 2014. Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. 23(2), 189–203.","ama":"Hosp J, Strüber M, Yanagawa Y, et al. Morpho-physiological criteria divide dentate gyrus interneurons into classes. Hippocampus. 2014;23(2):189-203. doi:10.1002/hipo.22214"},"publication":"Hippocampus","date_published":"2014-02-01T00:00:00Z","type":"journal_article","issue":"2","abstract":[{"text":"GABAergic inhibitory interneurons control fundamental aspects of neuronal network function. Their functional roles are assumed to be defined by the identity of their input synapses, the architecture of their dendritic tree, the passive and active membrane properties and finally the nature of their postsynaptic targets. Indeed, interneurons display a high degree of morphological and physiological heterogeneity. However, whether their morphological and physiological characteristics are correlated and whether interneuron diversity can be described by a continuum of GABAergic cell types or by distinct classes has remained unclear. Here we perform a detailed morphological and physiological characterization of GABAergic cells in the dentate gyrus, the input region of the hippocampus. To achieve an unbiased and efficient sampling and classification we used knock-in mice expressing the enhanced green fluorescent protein (eGFP) in glutamate decarboxylase 67 (GAD67)-positive neurons and performed cluster analysis. We identified five interneuron classes, each of them characterized by a distinct set of anatomical and physiological parameters. Cross-correlation analysis further revealed a direct relation between morphological and physiological properties indicating that dentate gyrus interneurons fall into functionally distinct classes which may differentially control neuronal network activity.","lang":"eng"}],"intvolume":" 23","ddc":["570"],"title":"Morpho-physiological criteria divide dentate gyrus interneurons into classes","status":"public","_id":"2285","user_id":"3FFCCD3A-F248-11E8-B48F-1D18A9856A87","file":[{"file_name":"IST-2016-461-v1+1_Hosp_et_al-2014-Hippocampus.pdf","access_level":"open_access","creator":"system","file_size":801589,"content_type":"application/pdf","file_id":"5178","relation":"main_file","date_created":"2018-12-12T10:15:54Z","date_updated":"2020-07-14T12:45:37Z","checksum":"ff6bc75a79dbc985a2e31b79253e6444"}],"oa_version":"Published Version","pubrep_id":"461"},{"publication_identifier":{"eissn":["1862-278X"],"issn":["0013-5585"]},"month":"08","doi":"10.1515/bmt-2013-4181","conference":{"location":"Graz, Austria","start_date":"2013-09-19","end_date":"2013-09-21","name":"BMT: Biomedizinische Technik "},"language":[{"iso":"eng"}],"oa":1,"external_id":{"pmid":["24042795"]},"quality_controlled":"1","file_date_updated":"2021-12-01T14:38:08Z","article_number":"000010151520134181","author":[{"id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-5621-8100","first_name":"Alois","last_name":"Schlögl","full_name":"Schlögl, Alois"},{"first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"},{"last_name":"Schmidt-Hieber","first_name":"C.","full_name":"Schmidt-Hieber, C."},{"last_name":"Guzman","first_name":"S. J.","full_name":"Guzman, S. J."}],"volume":58,"date_updated":"2021-12-02T12:51:12Z","date_created":"2021-12-01T14:35:35Z","pmid":1,"year":"2013","department":[{"_id":"PeJo"}],"publisher":"De Gruyter","publication_status":"published","article_processing_charge":"No","has_accepted_license":"1","day":"01","keyword":["biomedical engineering","data analysis","free software"],"date_published":"2013-08-01T00:00:00Z","citation":{"ista":"Schlögl A, Jonas PM, Schmidt-Hieber C, Guzman SJ. 2013. Stimfit: A fast visualization and analysis environment for cellular neurophysiology. Biomedical Engineering / Biomedizinische Technik. 58(SI-1-Track-G), 000010151520134181.","apa":"Schlögl, A., Jonas, P. M., Schmidt-Hieber, C., & Guzman, S. J. (2013). Stimfit: A fast visualization and analysis environment for cellular neurophysiology. Biomedical Engineering / Biomedizinische Technik. Graz, Austria: De Gruyter. https://doi.org/10.1515/bmt-2013-4181","ieee":"A. Schlögl, P. M. Jonas, C. Schmidt-Hieber, and S. J. Guzman, “Stimfit: A fast visualization and analysis environment for cellular neurophysiology,” Biomedical Engineering / Biomedizinische Technik, vol. 58, no. SI-1-Track-G. De Gruyter, 2013.","ama":"Schlögl A, Jonas PM, Schmidt-Hieber C, Guzman SJ. Stimfit: A fast visualization and analysis environment for cellular neurophysiology. Biomedical Engineering / Biomedizinische Technik. 2013;58(SI-1-Track-G). doi:10.1515/bmt-2013-4181","chicago":"Schlögl, Alois, Peter M Jonas, C. Schmidt-Hieber, and S. J. Guzman. “Stimfit: A Fast Visualization and Analysis Environment for Cellular Neurophysiology.” Biomedical Engineering / Biomedizinische Technik. De Gruyter, 2013. https://doi.org/10.1515/bmt-2013-4181.","mla":"Schlögl, Alois, et al. “Stimfit: A Fast Visualization and Analysis Environment for Cellular Neurophysiology.” Biomedical Engineering / Biomedizinische Technik, vol. 58, no. SI-1-Track-G, 000010151520134181, De Gruyter, 2013, doi:10.1515/bmt-2013-4181.","short":"A. Schlögl, P.M. Jonas, C. Schmidt-Hieber, S.J. Guzman, Biomedical Engineering / Biomedizinische Technik 58 (2013)."},"publication":"Biomedical Engineering / Biomedizinische Technik","article_type":"original","issue":"SI-1-Track-G","abstract":[{"lang":"eng","text":"Stimfit is a free cross-platform software package for viewing and analyzing electrophysiological data. It supports most standard file types for cellular neurophysiology and other biomedical formats. Its analysis algorithms have been used and validated in several experimental laboratories. Its embedded Python scripting interface makes Stimfit highly extensible and customizable."}],"type":"journal_article","file":[{"file_id":"10397","relation":"main_file","success":1,"checksum":"cdfc5339b530a25d6079f7223f0b1f16","date_updated":"2021-12-01T14:38:08Z","date_created":"2021-12-01T14:38:08Z","access_level":"open_access","file_name":"Schloegl_Abstract-BMT2013.pdf","creator":"schloegl","file_size":149825,"content_type":"application/pdf"}],"oa_version":"Submitted Version","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","_id":"10396","intvolume":" 58","ddc":["005","610"],"title":"Stimfit: A fast visualization and analysis environment for cellular neurophysiology","status":"public"},{"main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3471482/"}],"external_id":{"pmid":["23062335"]},"oa":1,"project":[{"name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","grant_number":"SFB-TR3-TP10B","_id":"25BDE9A4-B435-11E9-9278-68D0E5697425"}],"quality_controlled":"1","doi":"10.1016/j.bpj.2012.08.039","language":[{"iso":"eng"}],"month":"10","pmid":1,"acknowledgement":"This work was supported by the Deutsche Forschungsgemeinschaft (TR3/B10) and a European Research Council Advanced grant to P.J.\r\nWe thank H. Hu, S. J. Guzman, and C. Schmidt-Hieber for critically reading the manuscript, I. Koeva and F. Marr for technical support, and E. Kramberger for editorial assistance.\r\n","year":"2012","department":[{"_id":"PeJo"},{"_id":"ScienComp"}],"publisher":"Biophysical","publication_status":"published","author":[{"full_name":"Pernia-Andrade, Alejandro","id":"36963E98-F248-11E8-B48F-1D18A9856A87","last_name":"Pernia-Andrade","first_name":"Alejandro"},{"id":"3A578F32-F248-11E8-B48F-1D18A9856A87","first_name":"Sarit","last_name":"Goswami","full_name":"Goswami, Sarit"},{"first_name":"Yvonne","last_name":"Stickler","id":"63B76600-E9CC-11E9-9B5F-82450873F7A1","full_name":"Stickler, Yvonne"},{"first_name":"Ulrich","last_name":"Fröbe","full_name":"Fröbe, Ulrich"},{"first_name":"Alois","last_name":"Schlögl","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0002-5621-8100","full_name":"Schlögl, Alois"},{"full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","first_name":"Peter M","last_name":"Jonas"}],"volume":103,"date_created":"2018-12-11T12:00:32Z","date_updated":"2021-01-12T07:40:01Z","publist_id":"3774","citation":{"ama":"Pernia-Andrade A, Goswami S, Stickler Y, Fröbe U, Schlögl A, Jonas PM. A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. Biophysical Journal. 2012;103(7):1429-1439. doi:10.1016/j.bpj.2012.08.039","ista":"Pernia-Andrade A, Goswami S, Stickler Y, Fröbe U, Schlögl A, Jonas PM. 2012. A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. Biophysical Journal. 103(7), 1429–1439.","apa":"Pernia-Andrade, A., Goswami, S., Stickler, Y., Fröbe, U., Schlögl, A., & Jonas, P. M. (2012). A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo. Biophysical Journal. Biophysical. https://doi.org/10.1016/j.bpj.2012.08.039","ieee":"A. Pernia-Andrade, S. Goswami, Y. Stickler, U. Fröbe, A. Schlögl, and P. M. Jonas, “A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo,” Biophysical Journal, vol. 103, no. 7. Biophysical, pp. 1429–1439, 2012.","mla":"Pernia-Andrade, Alejandro, et al. “A Deconvolution Based Method with High Sensitivity and Temporal Resolution for Detection of Spontaneous Synaptic Currents in Vitro and in Vivo.” Biophysical Journal, vol. 103, no. 7, Biophysical, 2012, pp. 1429–39, doi:10.1016/j.bpj.2012.08.039.","short":"A. Pernia-Andrade, S. Goswami, Y. Stickler, U. Fröbe, A. Schlögl, P.M. Jonas, Biophysical Journal 103 (2012) 1429–1439.","chicago":"Pernia-Andrade, Alejandro, Sarit Goswami, Yvonne Stickler, Ulrich Fröbe, Alois Schlögl, and Peter M Jonas. “A Deconvolution Based Method with High Sensitivity and Temporal Resolution for Detection of Spontaneous Synaptic Currents in Vitro and in Vivo.” Biophysical Journal. Biophysical, 2012. https://doi.org/10.1016/j.bpj.2012.08.039."},"publication":"Biophysical Journal","page":"1429 - 1439","date_published":"2012-10-03T00:00:00Z","scopus_import":1,"day":"03","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"2954","intvolume":" 103","status":"public","title":"A deconvolution based method with high sensitivity and temporal resolution for detection of spontaneous synaptic currents in vitro and in vivo","oa_version":"Submitted Version","type":"journal_article","issue":"7","abstract":[{"text":"Spontaneous postsynaptic currents (PSCs) provide key information about the mechanisms of synaptic transmission and the activity modes of neuronal networks. However, detecting spontaneous PSCs in vitro and in vivo has been challenging, because of the small amplitude, the variable kinetics, and the undefined time of generation of these events. Here, we describe a, to our knowledge, new method for detecting spontaneous synaptic events by deconvolution, using a template that approximates the average time course of spontaneous PSCs. A recorded PSC trace is deconvolved from the template, resulting in a series of delta-like functions. The maxima of these delta-like events are reliably detected, revealing the precise onset times of the spontaneous PSCs. Among all detection methods, the deconvolution-based method has a unique temporal resolution, allowing the detection of individual events in high-frequency bursts. Furthermore, the deconvolution-based method has a high amplitude resolution, because deconvolution can substantially increase the signal/noise ratio. When tested against previously published methods using experimental data, the deconvolution-based method was superior for spontaneous PSCs recorded in vivo. Using the high-resolution deconvolution-based detection algorithm, we show that the frequency of spontaneous excitatory postsynaptic currents in dentate gyrus granule cells is 4.5 times higher in vivo than in vitro.","lang":"eng"}]},{"page":"14294 - 14304","publication":"Journal of Neuroscience","citation":{"apa":"Goswami, S., Bucurenciu, I., & Jonas, P. M. (2012). Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.6104-11.2012","ieee":"S. Goswami, I. Bucurenciu, and P. M. Jonas, “Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling,” Journal of Neuroscience, vol. 32, no. 41. Society for Neuroscience, pp. 14294–14304, 2012.","ista":"Goswami S, Bucurenciu I, Jonas PM. 2012. Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. Journal of Neuroscience. 32(41), 14294–14304.","ama":"Goswami S, Bucurenciu I, Jonas PM. Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. Journal of Neuroscience. 2012;32(41):14294-14304. doi:10.1523/JNEUROSCI.6104-11.2012","chicago":"Goswami, Sarit, Iancu Bucurenciu, and Peter M Jonas. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” Journal of Neuroscience. Society for Neuroscience, 2012. https://doi.org/10.1523/JNEUROSCI.6104-11.2012.","short":"S. Goswami, I. Bucurenciu, P.M. Jonas, Journal of Neuroscience 32 (2012) 14294–14304.","mla":"Goswami, Sarit, et al. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” Journal of Neuroscience, vol. 32, no. 41, Society for Neuroscience, 2012, pp. 14294–304, doi:10.1523/JNEUROSCI.6104-11.2012."},"date_published":"2012-10-10T00:00:00Z","scopus_import":1,"day":"10","status":"public","title":"Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling","intvolume":" 32","_id":"2969","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa_version":"Submitted Version","type":"journal_article","abstract":[{"lang":"eng","text":"The coupling between presynaptic Ca^(2+) channels and Ca^(2+) sensors of exocytosis is a key determinant of synaptic transmission. Evoked release from parvalbumin (PV)-expressing interneurons is triggered by nanodomain coupling of P/Q-type Ca^(2+) channels, whereas release from cholecystokinin (CCK)-containing interneurons is generated by microdomain coupling of N-type channels. Nanodomain coupling has several functional advantages, including speed and efficacy of transmission. One potential disadvantage is that stochastic\r\nopening of presynaptic Ca^(2+) channels may trigger spontaneous transmitter release. We addressed this possibility in rat hippocampal\r\ngranule cells, which receive converging inputs from different inhibitory sources. Both reduction of extracellular Ca^(2+) concentration and the unselective Ca^(2+) channel blocker Cd^(2+) reduced the frequency of miniature IPSCs (mIPSCs) in granule cells by ~50%, suggesting that the opening of presynaptic Ca^(2+) channels contributes to spontaneous release. Application of the selective P/Q-type Ca^(2+) channel blocker\r\nω-agatoxin IVa had no detectable effects, whereas both the N-type blocker ω-conotoxin GVIa and the L-type blocker nimodipine reduced\r\nmIPSC frequency. Furthermore, both the fast Ca^(2+) chelator BAPTA-AM and the slow chelator EGTA-AM reduced the mIPSC frequency,\r\nsuggesting that Ca^(2+)-dependent spontaneous release is triggered by microdomain rather than nanodomain coupling. The CB_(1) receptor\r\nagonist WIN 55212-2 also decreased spontaneous release; this effect was occluded by prior application of ω-conotoxin GVIa, suggesting that a major fraction of Ca^(2+)-dependent spontaneous release was generated at the terminals of CCK-expressing interneurons. Tonic inhibition generated by spontaneous opening of presynaptic N- and L-type Ca^(2+) channels may be important for hippocampal information processing.\r\n"}],"issue":"41","quality_controlled":"1","project":[{"_id":"25BDE9A4-B435-11E9-9278-68D0E5697425","grant_number":"SFB-TR3-TP10B","name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen"}],"main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632771/"}],"external_id":{"pmid":["23055500"]},"oa":1,"language":[{"iso":"eng"}],"doi":"10.1523/JNEUROSCI.6104-11.2012","month":"10","publication_status":"published","publisher":"Society for Neuroscience","department":[{"_id":"PeJo"}],"year":"2012","acknowledgement":"This work was supported by grants from the Deutsche Forschungsgemeinschaft (TR 3/B10, Leibniz program, GSC-4 Spemann Graduate School) and the European Union (European Research Council Advanced Grant).","pmid":1,"date_updated":"2021-01-12T07:40:08Z","date_created":"2018-12-11T12:00:36Z","volume":32,"author":[{"id":"3A578F32-F248-11E8-B48F-1D18A9856A87","first_name":"Sarit","last_name":"Goswami","full_name":"Goswami, Sarit"},{"full_name":"Bucurenciu, Iancu","first_name":"Iancu","last_name":"Bucurenciu"},{"full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804"}],"publist_id":"3744"},{"month":"09","language":[{"iso":"eng"}],"doi":"10.1038/nn.3162","quality_controlled":"1","main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3431448/"}],"oa":1,"external_id":{"pmid":["22842148"]},"publist_id":"3578","date_updated":"2021-01-12T07:41:12Z","date_created":"2018-12-11T12:01:30Z","volume":15,"author":[{"first_name":"Courtney","last_name":"Williams","full_name":"Williams, Courtney"},{"full_name":"Chen, Wenyan","first_name":"Wenyan","last_name":"Chen"},{"full_name":"Lee, Chia","last_name":"Lee","first_name":"Chia"},{"first_name":"Daniel","last_name":"Yaeger","full_name":"Yaeger, Daniel"},{"full_name":"Vyleta, Nicholas","id":"36C4978E-F248-11E8-B48F-1D18A9856A87","last_name":"Vyleta","first_name":"Nicholas"},{"last_name":"Smith","first_name":"Stephen","full_name":"Smith, Stephen"}],"publication_status":"published","department":[{"_id":"PeJo"}],"publisher":"Nature Publishing Group","year":"2012","acknowledgement":"The work was supported by the US National Institutes of Health (DA027110 and GM097433) and OCTRI. C.W. and N.P.V. were supported by a grant from the National Heart, Lung, and Blood Institute (T32HL033808).\r\nWe thank M. Andresen and K. Khodakhah for helpful comments. ","pmid":1,"day":"01","scopus_import":1,"date_published":"2012-09-01T00:00:00Z","page":"1195 - 1197","publication":"Nature Neuroscience","citation":{"apa":"Williams, C., Chen, W., Lee, C., Yaeger, D., Vyleta, N., & Smith, S. (2012). Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3162","ieee":"C. Williams, W. Chen, C. Lee, D. Yaeger, N. Vyleta, and S. Smith, “Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA,” Nature Neuroscience, vol. 15, no. 9. Nature Publishing Group, pp. 1195–1197, 2012.","ista":"Williams C, Chen W, Lee C, Yaeger D, Vyleta N, Smith S. 2012. Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. Nature Neuroscience. 15(9), 1195–1197.","ama":"Williams C, Chen W, Lee C, Yaeger D, Vyleta N, Smith S. Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA. Nature Neuroscience. 2012;15(9):1195-1197. doi:10.1038/nn.3162","chicago":"Williams, Courtney, Wenyan Chen, Chia Lee, Daniel Yaeger, Nicholas Vyleta, and Stephen Smith. “Coactivation of Multiple Tightly Coupled Calcium Channels Triggers Spontaneous Release of GABA.” Nature Neuroscience. Nature Publishing Group, 2012. https://doi.org/10.1038/nn.3162.","short":"C. Williams, W. Chen, C. Lee, D. Yaeger, N. Vyleta, S. Smith, Nature Neuroscience 15 (2012) 1195–1197.","mla":"Williams, Courtney, et al. “Coactivation of Multiple Tightly Coupled Calcium Channels Triggers Spontaneous Release of GABA.” Nature Neuroscience, vol. 15, no. 9, Nature Publishing Group, 2012, pp. 1195–97, doi:10.1038/nn.3162."},"abstract":[{"lang":"eng","text":"Voltage-activated Ca(2+) channels (VACCs) mediate Ca(2+) influx to trigger action potential-evoked neurotransmitter release, but the mechanism by which Ca(2+) regulates spontaneous transmission is unclear. We found that VACCs are the major physiological triggers for spontaneous release at mouse neocortical inhibitory synapses. Moreover, despite the absence of a synchronizing action potential, we found that spontaneous fusion of a GABA-containing vesicle required the activation of multiple tightly coupled VACCs of variable type."}],"issue":"9","type":"journal_article","oa_version":"Submitted Version","title":"Coactivation of multiple tightly coupled calcium channels triggers spontaneous release of GABA","status":"public","intvolume":" 15","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","_id":"3121"},{"publication":"Nature Reviews Neuroscience","citation":{"ama":"Eggermann E, Bucurenciu I, Goswami S, Jonas PM. Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. Nature Reviews Neuroscience. 2012;13(1):7-21. doi:10.1038/nrn3125","ista":"Eggermann E, Bucurenciu I, Goswami S, Jonas PM. 2012. Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. Nature Reviews Neuroscience. 13(1), 7–21.","apa":"Eggermann, E., Bucurenciu, I., Goswami, S., & Jonas, P. M. (2012). Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses. Nature Reviews Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nrn3125","ieee":"E. Eggermann, I. Bucurenciu, S. Goswami, and P. M. Jonas, “Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses,” Nature Reviews Neuroscience, vol. 13, no. 1. Nature Publishing Group, pp. 7–21, 2012.","mla":"Eggermann, Emmanuel, et al. “Nanodomain Coupling between Ca(2+) Channels and Sensors of Exocytosis at Fast Mammalian Synapses.” Nature Reviews Neuroscience, vol. 13, no. 1, Nature Publishing Group, 2012, pp. 7–21, doi:10.1038/nrn3125.","short":"E. Eggermann, I. Bucurenciu, S. Goswami, P.M. Jonas, Nature Reviews Neuroscience 13 (2012) 7–21.","chicago":"Eggermann, Emmanuel, Iancu Bucurenciu, Sarit Goswami, and Peter M Jonas. “Nanodomain Coupling between Ca(2+) Channels and Sensors of Exocytosis at Fast Mammalian Synapses.” Nature Reviews Neuroscience. Nature Publishing Group, 2012. https://doi.org/10.1038/nrn3125."},"page":"7 - 21","date_published":"2012-01-01T00:00:00Z","scopus_import":1,"day":"01","has_accepted_license":"1","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"3317","status":"public","title":"Nanodomain coupling between Ca(2+) channels and sensors of exocytosis at fast mammalian synapses","ddc":["570"],"intvolume":" 13","pubrep_id":"820","oa_version":"Submitted Version","file":[{"file_size":314246,"content_type":"application/pdf","creator":"system","access_level":"open_access","file_name":"IST-2017-820-v1+1_17463_3_art_file_109404_ltmxbw.pdf","checksum":"4c1c86b2f6e4e1562f5bb800b457ea9f","date_updated":"2020-07-14T12:46:07Z","date_created":"2018-12-12T10:12:13Z","relation":"main_file","file_id":"4931"},{"relation":"main_file","file_id":"4932","date_updated":"2020-07-14T12:46:07Z","date_created":"2018-12-12T10:12:14Z","checksum":"bceb2efdd49d115f4dde8486bc1be3f2","file_name":"IST-2017-820-v1+2_17463_3_figure_109402_ltmwlp.pdf","access_level":"open_access","file_size":1840216,"content_type":"application/pdf","creator":"system"}],"type":"journal_article","abstract":[{"lang":"eng","text":"The physical distance between presynaptic Ca2+ channels and the Ca2+ sensors that trigger exocytosis of neurotransmitter-containing vesicles is a key determinant of the signalling properties of synapses in the nervous system. Recent functional analysis indicates that in some fast central synapses, transmitter release is triggered by a small number of Ca2+ channels that are coupled to Ca2+ sensors at the nanometre scale. Molecular analysis suggests that this tight coupling is generated by protein–protein interactions involving Ca2+ channels, Ca2+ sensors and various other synaptic proteins. Nanodomain coupling has several functional advantages, as it increases the efficacy, speed and energy efficiency of synaptic transmission."}],"issue":"1","oa":1,"quality_controlled":"1","project":[{"name":"Synaptic Mechanisms of Neuronal Network Function","grant_number":"JO_780/A5","_id":"25BC64A8-B435-11E9-9278-68D0E5697425"},{"_id":"25BDE9A4-B435-11E9-9278-68D0E5697425","grant_number":"SFB-TR3-TP10B","name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen"}],"doi":"10.1038/nrn3125","language":[{"iso":"eng"}],"month":"01","acknowledgement":"Work of the authors was funded by grants of the Deutsche Forschungsgemeinschaft to P.J. (grants SFB 780/A5, TR 3/B10 and the Leibniz programme), a European Research Council Advanced grant to P.J. and a Swiss National Foundation fellowship to E.E.\r\nWe thank D. Tsien and E. Neher for their comments on this Review, J. Guzmán and A. Pernía-Andrade for reading earlier versions and E. Kramberger for perfect editorial support. We apologize that owing to space constraints, not all relevant papers could be cited.\r\n","year":"2012","publication_status":"published","department":[{"_id":"PeJo"}],"publisher":"Nature Publishing Group","author":[{"full_name":"Eggermann, Emmanuel","id":"34DACA34-E9AE-11E9-849C-D35BD8ADC20C","first_name":"Emmanuel","last_name":"Eggermann"},{"id":"4BD1D872-E9AE-11E9-9EE9-8BF4597A9E2A","last_name":"Bucurenciu","first_name":"Iancu","full_name":"Bucurenciu, Iancu"},{"id":"3A578F32-F248-11E8-B48F-1D18A9856A87","last_name":"Goswami","first_name":"Sarit","full_name":"Goswami, Sarit"},{"orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","first_name":"Peter M","full_name":"Jonas, Peter M"}],"date_created":"2018-12-11T12:02:38Z","date_updated":"2021-01-12T07:42:36Z","volume":13,"file_date_updated":"2020-07-14T12:46:07Z","publist_id":"3322"},{"publication":"Frontiers in Neuroscience","citation":{"ama":"Tangermann M, Müller K, Aertsen A, et al. Review of the BCI competition IV. Frontiers in Neuroscience. 2012;6. doi:10.3389/fnins.2012.00055","ista":"Tangermann M, Müller K, Aertsen A, Birbaumer N, Braun C, Brunner C, Leeb R, Mehring C, Miller K, Müller Putz G, Nolte G, Pfurtscheller G, Preissl H, Schalk G, Schlögl A, Vidaurre C, Waldert S, Blankertz B. 2012. Review of the BCI competition IV. Frontiers in Neuroscience. 6, 55.","ieee":"M. Tangermann et al., “Review of the BCI competition IV,” Frontiers in Neuroscience, vol. 6. Frontiers Research Foundation, 2012.","apa":"Tangermann, M., Müller, K., Aertsen, A., Birbaumer, N., Braun, C., Brunner, C., … Blankertz, B. (2012). Review of the BCI competition IV. Frontiers in Neuroscience. Frontiers Research Foundation. https://doi.org/10.3389/fnins.2012.00055","mla":"Tangermann, Michael, et al. “Review of the BCI Competition IV.” Frontiers in Neuroscience, vol. 6, 55, Frontiers Research Foundation, 2012, doi:10.3389/fnins.2012.00055.","short":"M. Tangermann, K. Müller, A. Aertsen, N. Birbaumer, C. Braun, C. Brunner, R. Leeb, C. Mehring, K. Miller, G. Müller Putz, G. Nolte, G. Pfurtscheller, H. Preissl, G. Schalk, A. Schlögl, C. Vidaurre, S. Waldert, B. Blankertz, Frontiers in Neuroscience 6 (2012).","chicago":"Tangermann, Michael, Klaus Müller, Ad Aertsen, Niels Birbaumer, Christoph Braun, Clemens Brunner, Robert Leeb, et al. “Review of the BCI Competition IV.” Frontiers in Neuroscience. Frontiers Research Foundation, 2012. https://doi.org/10.3389/fnins.2012.00055."},"date_published":"2012-07-13T00:00:00Z","scopus_import":1,"day":"13","has_accepted_license":"1","status":"public","ddc":["004"],"title":"Review of the BCI competition IV","intvolume":" 6","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","_id":"493","file":[{"checksum":"195238221c4b0b0f4035f6f6c16ea17c","date_updated":"2020-07-14T12:46:35Z","date_created":"2018-12-12T10:18:34Z","file_id":"5356","relation":"main_file","creator":"system","file_size":2693701,"content_type":"application/pdf","access_level":"open_access","file_name":"IST-2018-945-v1+1_2012_Schloegl_Review_of.pdf"}],"oa_version":"Published Version","pubrep_id":"945","type":"journal_article","abstract":[{"lang":"eng","text":"The BCI competition IV stands in the tradition of prior BCI competitions that aim to provide high quality neuroscientific data for open access to the scientific community. As experienced already in prior competitions not only scientists from the narrow field of BCI compete, but scholars with a broad variety of backgrounds and nationalities. They include high specialists as well as students.The goals of all BCI competitions have always been to challenge with respect to novel paradigms and complex data. We report on the following challenges: (1) asynchronous data, (2) synthetic, (3) multi-class continuous data, (4) sessionto-session transfer, (5) directionally modulated MEG, (6) finger movements recorded by ECoG. As after past competitions, our hope is that winning entries may enhance the analysis methods of future BCIs."}],"quality_controlled":"1","oa":1,"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"language":[{"iso":"eng"}],"doi":"10.3389/fnins.2012.00055","month":"07","publication_status":"published","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"publisher":"Frontiers Research Foundation","acknowledgement":"The studies were in part or completely supported by the Bundesministerium für Bildung und Forschung (BMBF), Fkz 01IB001A, 01GQ0850, by the German Science Foundation (DFG, contract MU 987/3-2), by the European ICT Programme Projects FP7-224631 and 216886, the World Class University Program through the National Research Foundation of Korea funded by the Ministry of Education, Science, and Technology (Grant R31-10008), the US Army Research Office [W911NF-08-1-0216 (Gerwin Schalk) and W911NF-07-1-0415 (Gerwin Schalk)] and the NIH [EB006356 (Gerwin Schalk) and EB000856 (Gerwin Schalk), the WIN-Kolleg of the Heidelberg Academy of Sciences and Humanities, German Federal Ministry of Education and Research grants 01GQ0420, 01GQ0761, 01GQ0762, and 01GQ0830, German Research Foundation grants 550/B5 and C6, and by a scholarship from the German National Academic Foundation. This paper only reflects the authors’ views and funding agencies are not liable for any use that may be made of the information contained herein.\r\n","year":"2012","date_created":"2018-12-11T11:46:46Z","date_updated":"2021-01-12T08:01:03Z","volume":6,"author":[{"full_name":"Tangermann, Michael","last_name":"Tangermann","first_name":"Michael"},{"full_name":"Müller, Klaus","first_name":"Klaus","last_name":"Müller"},{"first_name":"Ad","last_name":"Aertsen","full_name":"Aertsen, Ad"},{"full_name":"Birbaumer, Niels","first_name":"Niels","last_name":"Birbaumer"},{"first_name":"Christoph","last_name":"Braun","full_name":"Braun, Christoph"},{"first_name":"Clemens","last_name":"Brunner","full_name":"Brunner, Clemens"},{"first_name":"Robert","last_name":"Leeb","full_name":"Leeb, Robert"},{"full_name":"Mehring, Carsten","first_name":"Carsten","last_name":"Mehring"},{"last_name":"Miller","first_name":"Kai","full_name":"Miller, Kai"},{"first_name":"Gernot","last_name":"Müller Putz","full_name":"Müller Putz, Gernot"},{"last_name":"Nolte","first_name":"Guido","full_name":"Nolte, Guido"},{"full_name":"Pfurtscheller, Gert","first_name":"Gert","last_name":"Pfurtscheller"},{"last_name":"Preissl","first_name":"Hubert","full_name":"Preissl, Hubert"},{"last_name":"Schalk","first_name":"Gerwin","full_name":"Schalk, Gerwin"},{"full_name":"Schlögl, Alois","orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","last_name":"Schlögl","first_name":"Alois"},{"first_name":"Carmen","last_name":"Vidaurre","full_name":"Vidaurre, Carmen"},{"full_name":"Waldert, Stephan","first_name":"Stephan","last_name":"Waldert"},{"last_name":"Blankertz","first_name":"Benjamin","full_name":"Blankertz, Benjamin"}],"article_number":"55","file_date_updated":"2020-07-14T12:46:35Z","publist_id":"7327"},{"page":"600 - 606","article_type":"original","citation":{"chicago":"Kim, Sooyun, José Guzmán, Hua Hu, and Peter M Jonas. “Active Dendrites Support Efficient Initiation of Dendritic Spikes in Hippocampal CA3 Pyramidal Neurons.” Nature Neuroscience. Nature Publishing Group, 2012. https://doi.org/10.1038/nn.3060.","short":"S. Kim, J. Guzmán, H. Hu, P.M. Jonas, Nature Neuroscience 15 (2012) 600–606.","mla":"Kim, Sooyun, et al. “Active Dendrites Support Efficient Initiation of Dendritic Spikes in Hippocampal CA3 Pyramidal Neurons.” Nature Neuroscience, vol. 15, no. 4, Nature Publishing Group, 2012, pp. 600–06, doi:10.1038/nn.3060.","ieee":"S. Kim, J. Guzmán, H. Hu, and P. M. Jonas, “Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons,” Nature Neuroscience, vol. 15, no. 4. Nature Publishing Group, pp. 600–606, 2012.","apa":"Kim, S., Guzmán, J., Hu, H., & Jonas, P. M. (2012). Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3060","ista":"Kim S, Guzmán J, Hu H, Jonas PM. 2012. Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. Nature Neuroscience. 15(4), 600–606.","ama":"Kim S, Guzmán J, Hu H, Jonas PM. Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons. Nature Neuroscience. 2012;15(4):600-606. doi:10.1038/nn.3060"},"publication":"Nature Neuroscience","date_published":"2012-04-01T00:00:00Z","scopus_import":"1","article_processing_charge":"No","day":"01","intvolume":" 15","title":"Active dendrites support efficient initiation of dendritic spikes in hippocampal CA3 pyramidal neurons","status":"public","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","_id":"3258","oa_version":"Published Version","type":"journal_article","issue":"4","abstract":[{"lang":"eng","text":"CA3 pyramidal neurons are important for memory formation and pattern completion in the hippocampal network. It is generally thought that proximal synapses from the mossy fibers activate these neurons most efficiently, whereas distal inputs from the perforant path have a weaker modulatory influence. We used confocally targeted patch-clamp recording from dendrites and axons to map the activation of rat CA3 pyramidal neurons at the subcellular level. Our results reveal two distinct dendritic domains. In the proximal domain, action potentials initiated in the axon backpropagate actively with large amplitude and fast time course. In the distal domain, Na+ channel–mediated dendritic spikes are efficiently initiated by waveforms mimicking synaptic events. CA3 pyramidal neuron dendrites showed a high Na+-to-K+ conductance density ratio, providing ideal conditions for active backpropagation and dendritic spike initiation. Dendritic spikes may enhance the computational power of CA3 pyramidal neurons in the hippocampal network."}],"project":[{"_id":"25BDE9A4-B435-11E9-9278-68D0E5697425","grant_number":"SFB-TR3-TP10B","name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen"}],"quality_controlled":"1","oa":1,"external_id":{"pmid":["22388958"]},"main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3617474/","open_access":"1"}],"language":[{"iso":"eng"}],"doi":"10.1038/nn.3060","publication_identifier":{"issn":["1546-1726"]},"month":"04","publisher":"Nature Publishing Group","department":[{"_id":"PeJo"}],"publication_status":"published","pmid":1,"year":"2012","acknowledgement":"This work was supported by the Deutsche Forschungsgemeinschaft (TR 3/B10) and the European Union (European Research Council Advanced grant to P.J.).","volume":15,"date_created":"2018-12-11T12:02:18Z","date_updated":"2023-09-07T11:43:52Z","related_material":{"record":[{"id":"2964","relation":"dissertation_contains","status":"public"}]},"author":[{"full_name":"Kim, Sooyun","id":"394AB1C8-F248-11E8-B48F-1D18A9856A87","first_name":"Sooyun","last_name":"Kim"},{"full_name":"Guzmán, José","last_name":"Guzmán","first_name":"José","orcid":"0000-0003-2209-5242","id":"30CC5506-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Hu, Hua","first_name":"Hua","last_name":"Hu","id":"4AC0145C-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804"}],"publist_id":"3390"},{"article_processing_charge":"No","publication_identifier":{"issn":["2663-337X"]},"month":"06","day":"01","page":"65","citation":{"ama":"Kim S. Active properties of hippocampal CA3 pyramidal neuron dendrites. 2012.","ieee":"S. Kim, “Active properties of hippocampal CA3 pyramidal neuron dendrites,” Institute of Science and Technology Austria, 2012.","apa":"Kim, S. (2012). Active properties of hippocampal CA3 pyramidal neuron dendrites. Institute of Science and Technology Austria.","ista":"Kim S. 2012. Active properties of hippocampal CA3 pyramidal neuron dendrites. Institute of Science and Technology Austria.","short":"S. Kim, Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites, Institute of Science and Technology Austria, 2012.","mla":"Kim, Sooyun. Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites. Institute of Science and Technology Austria, 2012.","chicago":"Kim, Sooyun. “Active Properties of Hippocampal CA3 Pyramidal Neuron Dendrites.” Institute of Science and Technology Austria, 2012."},"language":[{"iso":"eng"}],"degree_awarded":"PhD","supervisor":[{"last_name":"Jonas","first_name":"Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M"}],"date_published":"2012-06-01T00:00:00Z","alternative_title":["ISTA Thesis"],"type":"dissertation","publist_id":"3755","abstract":[{"text":"CA3 pyramidal neurons are important for memory formation and pattern completion in the hippocampal network. These neurons receive multiple excitatory inputs from numerous sources. Therefore, the rules of spatiotemporal integration of multiple synaptic inputs and propagation of action potentials are important to understand how CA3 neurons contribute to higher brain functions at cellular level. By using confocally targeted patch-clamp recording techniques, we investigated the biophysical properties of rat CA3 pyramidal neuron dendrites. We found two distinct dendritic domains critical for action potential initiation and propagation: In the proximal domain, action potentials initiated in the axon backpropagate actively with large amplitude and fast time course. In the distal domain, Na+-channel mediated dendritic spikes are efficiently evoked by local dendritic depolarization or waveforms mimicking synaptic events. These findings can be explained by a high Na+-to-K+ conductance density ratio of CA3 pyramidal neuron dendrites. The results challenge the prevailing view that proximal mossy fiber inputs activate CA3 pyramidal neurons more efficiently than distal perforant inputs by showing that the distal synapses trigger a different form of activity represented by dendritic spikes. The high probability of dendritic spike initiation in the distal area may enhance the computational power of CA3 pyramidal neurons in the hippocampal network. ","lang":"eng"}],"department":[{"_id":"PeJo"},{"_id":"GradSch"}],"publisher":"Institute of Science and Technology Austria","status":"public","title":"Active properties of hippocampal CA3 pyramidal neuron dendrites","publication_status":"published","_id":"2964","year":"2012","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","oa_version":"None","date_updated":"2023-09-07T11:43:51Z","date_created":"2018-12-11T12:00:35Z","related_material":{"record":[{"relation":"part_of_dissertation","status":"public","id":"3258"}]},"author":[{"full_name":"Kim, Sooyun","id":"394AB1C8-F248-11E8-B48F-1D18A9856A87","last_name":"Kim","first_name":"Sooyun"}]},{"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","_id":"3318","year":"2011","title":"How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses","publication_status":"published","status":"public","intvolume":" 15","publisher":"Nature Publishing Group","department":[{"_id":"PeJo"}],"author":[{"full_name":"Eggermann, Emmanuel","last_name":"Eggermann","first_name":"Emmanuel"},{"first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"date_updated":"2021-01-12T07:42:37Z","date_created":"2018-12-11T12:02:38Z","oa_version":"Submitted Version","volume":15,"type":"journal_article","abstract":[{"text":"Parvalbumin is thought to act in a manner similar to EGTA, but how a slow Ca2+ buffer affects nanodomain-coupling regimes at GABAergic synapses is unclear. Direct measurements of parvalbumin concentration and paired recordings in rodent hippocampus and cerebellum revealed that parvalbumin affects synaptic dynamics only when expressed at high levels. Modeling suggests that, in high concentrations, parvalbumin may exert BAPTA-like effects, modulating nanodomain coupling via competition with local saturation of endogenous fixed buffers.","lang":"eng"}],"publist_id":"3321","publication":"Nature Neuroscience","citation":{"ista":"Eggermann E, Jonas PM. 2011. How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature Neuroscience. 15, 20–22.","apa":"Eggermann, E., & Jonas, P. M. (2011). How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature Neuroscience. Nature Publishing Group. https://doi.org/10.1038/nn.3002","ieee":"E. Eggermann and P. M. Jonas, “How the ‘slow’ Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses,” Nature Neuroscience, vol. 15. Nature Publishing Group, pp. 20–22, 2011.","ama":"Eggermann E, Jonas PM. How the “slow” Ca(2+) buffer parvalbumin affects transmitter release in nanodomain coupling regimes at GABAergic synapses. Nature Neuroscience. 2011;15:20-22. doi:10.1038/nn.3002","chicago":"Eggermann, Emmanuel, and Peter M Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.” Nature Neuroscience. Nature Publishing Group, 2011. https://doi.org/10.1038/nn.3002.","mla":"Eggermann, Emmanuel, and Peter M. Jonas. “How the ‘Slow’ Ca(2+) Buffer Parvalbumin Affects Transmitter Release in Nanodomain Coupling Regimes at GABAergic Synapses.” Nature Neuroscience, vol. 15, Nature Publishing Group, 2011, pp. 20–22, doi:10.1038/nn.3002.","short":"E. Eggermann, P.M. Jonas, Nature Neuroscience 15 (2011) 20–22."},"main_file_link":[{"url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3631701/","open_access":"1"}],"oa":1,"quality_controlled":"1","page":"20 - 22","date_published":"2011-12-04T00:00:00Z","doi":"10.1038/nn.3002","language":[{"iso":"eng"}],"scopus_import":1,"month":"12","day":"04"},{"language":[{"iso":"eng"}],"doi":"10.1016/j.neuron.2011.01.010","date_published":"2011-01-27T00:00:00Z","page":"185 - 187","quality_controlled":"1","citation":{"mla":"Pernia-Andrade, Alejandro, and Peter M. Jonas. “The Multiple Faces of RIM.” Neuron, vol. 69, no. 2, Elsevier, 2011, pp. 185–87, doi:10.1016/j.neuron.2011.01.010.","short":"A. Pernia-Andrade, P.M. Jonas, Neuron 69 (2011) 185–187.","chicago":"Pernia-Andrade, Alejandro, and Peter M Jonas. “The Multiple Faces of RIM.” Neuron. Elsevier, 2011. https://doi.org/10.1016/j.neuron.2011.01.010.","ama":"Pernia-Andrade A, Jonas PM. The multiple faces of RIM. Neuron. 2011;69(2):185-187. doi:10.1016/j.neuron.2011.01.010","ista":"Pernia-Andrade A, Jonas PM. 2011. The multiple faces of RIM. Neuron. 69(2), 185–187.","ieee":"A. Pernia-Andrade and P. M. Jonas, “The multiple faces of RIM,” Neuron, vol. 69, no. 2. Elsevier, pp. 185–187, 2011.","apa":"Pernia-Andrade, A., & Jonas, P. M. (2011). The multiple faces of RIM. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2011.01.010"},"publication":"Neuron","day":"27","month":"01","scopus_import":1,"oa_version":"None","volume":69,"date_created":"2018-12-11T12:02:56Z","date_updated":"2021-01-12T07:43:00Z","author":[{"id":"36963E98-F248-11E8-B48F-1D18A9856A87","last_name":"Pernia-Andrade","first_name":"Alejandro","full_name":"Pernia-Andrade, Alejandro"},{"full_name":"Jonas, Peter M","last_name":"Jonas","first_name":"Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"publisher":"Elsevier","department":[{"_id":"PeJo"}],"intvolume":" 69","title":"The multiple faces of RIM","status":"public","publication_status":"published","_id":"3369","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","year":"2011","publist_id":"3243","issue":"2","abstract":[{"text":"Rab3 interacting molecules (RIMs) are highly enriched in the active zones of presynaptic terminals. It is generally thought that they operate as effectors of the small G protein Rab3. Three recent papers, by Han et al. (this issue of Neuron), Deng et al. (this issue of Neuron), and Kaeser et al. (a recent issue of Cell), shed new light on the functional role of RIM in presynaptic terminals. First, RIM tethers Ca2+ channels to active zones. Second, RIM contributes to priming of synaptic vesicles by interacting with another presynaptic protein, Munc13.","lang":"eng"}],"type":"journal_article"},{"month":"03","day":"23","scopus_import":1,"language":[{"iso":"eng"}],"date_published":"2011-03-23T00:00:00Z","doi":"10.1523/JNEUROSCI.6398-10.2011","page":"4593 - 4606","quality_controlled":"1","oa":1,"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3097128/"}],"citation":{"ista":"Vyleta N, Smith S. 2011. Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. European Journal of Neuroscience. 31(12), 4593–4606.","ieee":"N. Vyleta and S. Smith, “Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor,” European Journal of Neuroscience, vol. 31, no. 12. Wiley-Blackwell, pp. 4593–4606, 2011.","apa":"Vyleta, N., & Smith, S. (2011). Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. European Journal of Neuroscience. Wiley-Blackwell. https://doi.org/10.1523/JNEUROSCI.6398-10.2011","ama":"Vyleta N, Smith S. Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor. European Journal of Neuroscience. 2011;31(12):4593-4606. doi:10.1523/JNEUROSCI.6398-10.2011","chicago":"Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” European Journal of Neuroscience. Wiley-Blackwell, 2011. https://doi.org/10.1523/JNEUROSCI.6398-10.2011.","mla":"Vyleta, Nicholas, and Stephen Smith. “Spontaneous Glutamate Release Is Independent of Calcium Influx and Tonically Activated by the Calcium-Sensing Receptor.” European Journal of Neuroscience, vol. 31, no. 12, Wiley-Blackwell, 2011, pp. 4593–606, doi:10.1523/JNEUROSCI.6398-10.2011.","short":"N. Vyleta, S. Smith, European Journal of Neuroscience 31 (2011) 4593–4606."},"publication":"European Journal of Neuroscience","publist_id":"7353","issue":"12","abstract":[{"lang":"eng","text":"Spontaneous release of glutamate is important for maintaining synaptic strength and controlling spike timing in the brain. Mechanisms regulating spontaneous exocytosis remain poorly understood. Extracellular calcium concentration ([Ca2+]o) regulates Ca2+ entry through voltage-activated calcium channels (VACCs) and consequently is a pivotal determinant of action potential-evoked vesicle fusion. Extracellular Ca 2+ also enhances spontaneous release, but via unknown mechanisms. Here we report that external Ca2+ triggers spontaneous glutamate release more weakly than evoked release in mouse neocortical neurons. Blockade of VACCs has no effect on the spontaneous release rate or its dependence on [Ca2+]o. Intracellular [Ca2+] slowly increases in a minority of neurons following increases in [Ca2+]o. Furthermore, the enhancement of spontaneous release by extracellular calcium is insensitive to chelation of intracellular calcium by BAPTA. Activation of the calcium-sensing receptor (CaSR), a G-protein-coupled receptor present in nerve terminals, by several specific agonists increased spontaneous glutamate release. The frequency of spontaneous synaptic transmission was decreased in CaSR mutant neurons. The concentration-effect relationship for extracellular calcium regulation of spontaneous release was well described by a combination of CaSR-dependent and CaSR-independent mechanisms. Overall these results indicate that extracellular Ca2+ does not trigger spontaneous glutamate release by simply increasing calcium influx but stimulates CaSR and thereby promotes resting spontaneous glutamate release. "}],"type":"journal_article","oa_version":"Submitted Version","volume":31,"date_updated":"2021-01-12T08:00:49Z","date_created":"2018-12-11T11:46:39Z","author":[{"last_name":"Vyleta","first_name":"Nicholas","id":"36C4978E-F248-11E8-B48F-1D18A9856A87","full_name":"Vyleta, Nicholas"},{"full_name":"Smith, Stephen","first_name":"Stephen","last_name":"Smith"}],"intvolume":" 31","department":[{"_id":"PeJo"}],"publisher":"Wiley-Blackwell","publication_status":"published","status":"public","title":"Spontaneous glutamate release is independent of calcium influx and tonically activated by the calcium-sensing receptor","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","_id":"469","year":"2011"},{"date_published":"2011-01-01T00:00:00Z","publication":"Computational Intelligence and Neuroscience","citation":{"short":"A. Schlögl, C. Vidaurre, T. Sander, Computational Intelligence and Neuroscience 2011 (2011).","mla":"Schlögl, Alois, et al. “BioSig: The Free and Open Source Software Library for Biomedical Signal Processing.” Computational Intelligence and Neuroscience, vol. 2011, 935364, Hindawi Publishing Corporation, 2011, doi:10.1155/2011/935364.","chicago":"Schlögl, Alois, Carmen Vidaurre, and Tilmann Sander. “BioSig: The Free and Open Source Software Library for Biomedical Signal Processing.” Computational Intelligence and Neuroscience. Hindawi Publishing Corporation, 2011. https://doi.org/10.1155/2011/935364.","ama":"Schlögl A, Vidaurre C, Sander T. BioSig: The free and open source software library for biomedical signal processing. Computational Intelligence and Neuroscience. 2011;2011. doi:10.1155/2011/935364","apa":"Schlögl, A., Vidaurre, C., & Sander, T. (2011). BioSig: The free and open source software library for biomedical signal processing. Computational Intelligence and Neuroscience. Hindawi Publishing Corporation. https://doi.org/10.1155/2011/935364","ieee":"A. Schlögl, C. Vidaurre, and T. Sander, “BioSig: The free and open source software library for biomedical signal processing,” Computational Intelligence and Neuroscience, vol. 2011. Hindawi Publishing Corporation, 2011.","ista":"Schlögl A, Vidaurre C, Sander T. 2011. BioSig: The free and open source software library for biomedical signal processing. Computational Intelligence and Neuroscience. 2011, 935364."},"day":"01","has_accepted_license":"1","scopus_import":1,"pubrep_id":"947","oa_version":"Published Version","file":[{"checksum":"8263bbf255171f2054f43f3db5f53b6e","date_created":"2018-12-12T10:07:44Z","date_updated":"2020-07-14T12:46:35Z","file_id":"4642","relation":"main_file","creator":"system","content_type":"application/pdf","file_size":2863551,"access_level":"open_access","file_name":"IST-2018-947-v1+1_2011_Schloegl_BioSig.pdf"}],"user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","_id":"490","status":"public","title":"BioSig: The free and open source software library for biomedical signal processing","ddc":["005"],"intvolume":" 2011","abstract":[{"lang":"eng","text":"BioSig is an open source software library for biomedical signal processing. The aim of the BioSig project is to foster research in biomedical signal processing by providing free and open source software tools for many different application areas. Some of the areas where BioSig can be employed are neuroinformatics, brain-computer interfaces, neurophysiology, psychology, cardiovascular systems, and sleep research. Moreover, the analysis of biosignals such as the electroencephalogram (EEG), electrocorticogram (ECoG), electrocardiogram (ECG), electrooculogram (EOG), electromyogram (EMG), or respiration signals is a very relevant element of the BioSig project. Specifically, BioSig provides solutions for data acquisition, artifact processing, quality control, feature extraction, classification, modeling, and data visualization, to name a few. In this paper, we highlight several methods to help students and researchers to work more efficiently with biomedical signals. "}],"type":"journal_article","doi":"10.1155/2011/935364","language":[{"iso":"eng"}],"tmp":{"name":"Creative Commons Attribution 4.0 International Public License (CC-BY 4.0)","legal_code_url":"https://creativecommons.org/licenses/by/4.0/legalcode","short":"CC BY (4.0)","image":"/images/cc_by.png"},"oa":1,"quality_controlled":"1","month":"01","author":[{"full_name":"Schlögl, Alois","last_name":"Schlögl","first_name":"Alois","orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Vidaurre, Carmen","last_name":"Vidaurre","first_name":"Carmen"},{"full_name":"Sander, Tilmann","first_name":"Tilmann","last_name":"Sander"}],"date_updated":"2021-01-12T08:01:02Z","date_created":"2018-12-11T11:46:45Z","volume":2011,"year":"2011","publication_status":"published","publisher":"Hindawi Publishing Corporation","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"file_date_updated":"2020-07-14T12:46:35Z","publist_id":"7330","article_number":"935364"},{"type":"journal_article","publist_id":"2512","issue":"6","abstract":[{"text":"Long-term depression (LTD) is a form of synaptic plasticity that may contribute to information storage in the central nervous system. Here we report that LTD can be elicited in layer 5 pyramidal neurons of the rat prefrontal cortex by pairing low frequency stimulation with a modest postsynaptic depolarization. The induction of LTD required the activation of both metabotropic glutamate receptors of the mGlu1 subtype and voltage-sensitive Ca(2+) channels (VSCCs) of the T/R, P/Q and N types, leading to the stimulation of intracellular inositol trisphosphate (IP3) receptors by IP3 and Ca(2+). The subsequent release of Ca(2+) from intracellular stores activated the protein phosphatase cascade involving calcineurin and protein phosphatase 1. The activation of purinergic P2Y(1) receptors blocked LTD. This effect was prevented by P2Y(1) receptor antagonists and was absent in mice lacking P2Y(1) but not P2Y(2) receptors. We also found that activation of P2Y(1) receptors inhibits Ca(2+) transients via VSCCs in the apical dendrites and spines of pyramidal neurons. In addition, we show that the release of ATP under hypoxia is able to inhibit LTD by acting on postsynaptic P2Y(1) receptors. In conclusion, these data suggest that the reduction of Ca(2+) influx via VSCCs caused by the activation of P2Y(1) receptors by ATP is the possible mechanism for the inhibition of LTD in prefrontal cortex.","lang":"eng"}],"department":[{"_id":"PeJo"}],"publisher":"Elsevier","intvolume":" 59","status":"public","publication_status":"published","title":"P2Y1 receptors inhibit long-term depression in the prefrontal cortex.","_id":"3718","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","acknowledgement":" The financial support of the Deutsche Forschungsgemeinschaft (IL 20/12-1, KI 677/2-4) is gratefully acknowledged.\r\nWe thank B. H. Koller (Department of Genetics and Molecular Biology, University of North Carolina at Chapel Hill, NC, USA) for the generous supply of P2Y1−/− and P2Y2−/− mice. We are grateful to Dr. A. Schulz for reanalysing the genotype of the P2Y1−/− mice. The authors thank P. Jonas and U. Heinemann for many helpful comments and A-K. Krause, L Feige and M. Eberts for their excellent technical support.","year":"2010","volume":59,"oa_version":"None","date_updated":"2021-01-12T07:51:42Z","date_created":"2018-12-11T12:04:47Z","author":[{"full_name":"Guzmán, José","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","last_name":"Guzmán","first_name":"José"},{"last_name":"Schmidt","first_name":"Hartmut","full_name":"Schmidt, Hartmut"},{"full_name":"Franke, Heike","last_name":"Franke","first_name":"Heike"},{"full_name":"Krügel, Ute","last_name":"Krügel","first_name":"Ute"},{"last_name":"Eilers","first_name":"Jens","full_name":"Eilers, Jens"},{"last_name":"Illes","first_name":"Peter","full_name":"Illes, Peter"},{"full_name":"Gerevich, Zoltan","first_name":"Zoltan","last_name":"Gerevich"}],"scopus_import":1,"day":"01","month":"11","page":"406 - 415","quality_controlled":"1","citation":{"mla":"Guzmán, José, et al. “P2Y1 Receptors Inhibit Long-Term Depression in the Prefrontal Cortex.” Neuropharmacology, vol. 59, no. 6, Elsevier, 2010, pp. 406–15, doi:10.1016/j.neuropharm.2010.05.013.","short":"J. Guzmán, H. Schmidt, H. Franke, U. Krügel, J. Eilers, P. Illes, Z. Gerevich, Neuropharmacology 59 (2010) 406–415.","chicago":"Guzmán, José, Hartmut Schmidt, Heike Franke, Ute Krügel, Jens Eilers, Peter Illes, and Zoltan Gerevich. “P2Y1 Receptors Inhibit Long-Term Depression in the Prefrontal Cortex.” Neuropharmacology. Elsevier, 2010. https://doi.org/10.1016/j.neuropharm.2010.05.013.","ama":"Guzmán J, Schmidt H, Franke H, et al. P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology. 2010;59(6):406-415. doi:10.1016/j.neuropharm.2010.05.013","ista":"Guzmán J, Schmidt H, Franke H, Krügel U, Eilers J, Illes P, Gerevich Z. 2010. P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology. 59(6), 406–415.","ieee":"J. Guzmán et al., “P2Y1 receptors inhibit long-term depression in the prefrontal cortex.,” Neuropharmacology, vol. 59, no. 6. Elsevier, pp. 406–415, 2010.","apa":"Guzmán, J., Schmidt, H., Franke, H., Krügel, U., Eilers, J., Illes, P., & Gerevich, Z. (2010). P2Y1 receptors inhibit long-term depression in the prefrontal cortex. Neuropharmacology. Elsevier. https://doi.org/10.1016/j.neuropharm.2010.05.013"},"publication":"Neuropharmacology","language":[{"iso":"eng"}],"date_published":"2010-11-01T00:00:00Z","doi":"10.1016/j.neuropharm.2010.05.013"},{"oa_version":"Published Version","title":"Beyond TARPs: The growing list of auxiliary AMPAR subunits","status":"public","intvolume":" 66","_id":"3832","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","abstract":[{"lang":"eng","text":"A recent paper by von Engelhardt et al. identifies a novel auxiliary subunit of native AMPARs, termedCKAMP44. Unlike other auxiliary subunits, CKAMP44 accelerates desensitization and prolongs recovery from desensitization. CKAMP44 is highly expressed in hippocampal dentate gyrus granule cells and decreases the paired-pulse ratio at perforant path input synapses. Thus, both principal and auxiliary AMPAR subunits control the time course of signaling at glutamatergic synapses."}],"issue":"1","type":"journal_article","date_published":"2010-04-15T00:00:00Z","page":"8 - 10","publication":"Neuron","citation":{"ama":"Guzmán J, Jonas PM. Beyond TARPs: The growing list of auxiliary AMPAR subunits. Neuron. 2010;66(1):8-10. doi:10.1016/j.neuron.2010.04.003","apa":"Guzmán, J., & Jonas, P. M. (2010). Beyond TARPs: The growing list of auxiliary AMPAR subunits. Neuron. Elsevier. https://doi.org/10.1016/j.neuron.2010.04.003","ieee":"J. Guzmán and P. M. Jonas, “Beyond TARPs: The growing list of auxiliary AMPAR subunits,” Neuron, vol. 66, no. 1. Elsevier, pp. 8–10, 2010.","ista":"Guzmán J, Jonas PM. 2010. Beyond TARPs: The growing list of auxiliary AMPAR subunits. Neuron. 66(1), 8–10.","short":"J. Guzmán, P.M. Jonas, Neuron 66 (2010) 8–10.","mla":"Guzmán, José, and Peter M. Jonas. “Beyond TARPs: The Growing List of Auxiliary AMPAR Subunits.” Neuron, vol. 66, no. 1, Elsevier, 2010, pp. 8–10, doi:10.1016/j.neuron.2010.04.003.","chicago":"Guzmán, José, and Peter M Jonas. “Beyond TARPs: The Growing List of Auxiliary AMPAR Subunits.” Neuron. Elsevier, 2010. https://doi.org/10.1016/j.neuron.2010.04.003."},"day":"15","article_processing_charge":"No","scopus_import":1,"date_updated":"2021-01-12T07:52:31Z","date_created":"2018-12-11T12:05:25Z","volume":66,"author":[{"full_name":"Guzmán, José","first_name":"José","last_name":"Guzmán","id":"30CC5506-F248-11E8-B48F-1D18A9856A87"},{"orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","first_name":"Peter M","full_name":"Jonas, Peter M"}],"publication_status":"published","department":[{"_id":"PeJo"}],"publisher":"Elsevier","year":"2010","pmid":1,"publist_id":"2377","language":[{"iso":"eng"}],"doi":"10.1016/j.neuron.2010.04.003","quality_controlled":"1","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pubmed/20399724"}],"oa":1,"external_id":{"pmid":["20399724"]},"month":"04"},{"quality_controlled":"1","page":"1194 - 1195","publication":"The European Journal of Neuroscience","citation":{"mla":"Jonas, Peter M., and Stefan Hefft. “GABA Release at Terminals of CCK-Interneurons: Synchrony, Asynchrony and Modulation by Cannabinoid Receptors (Commentary on Ali & Todorova).” The European Journal of Neuroscience, vol. 31, no. 7, Wiley-Blackwell, 2010, pp. 1194–95, doi:10.1111/j.1460-9568.2010.07189.x.","short":"P.M. Jonas, S. Hefft, The European Journal of Neuroscience 31 (2010) 1194–1195.","chicago":"Jonas, Peter M, and Stefan Hefft. “GABA Release at Terminals of CCK-Interneurons: Synchrony, Asynchrony and Modulation by Cannabinoid Receptors (Commentary on Ali & Todorova).” The European Journal of Neuroscience. Wiley-Blackwell, 2010. https://doi.org/10.1111/j.1460-9568.2010.07189.x.","ama":"Jonas PM, Hefft S. GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova). The European Journal of Neuroscience. 2010;31(7):1194-1195. doi:10.1111/j.1460-9568.2010.07189.x","ista":"Jonas PM, Hefft S. 2010. GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova). The European Journal of Neuroscience. 31(7), 1194–1195.","apa":"Jonas, P. M., & Hefft, S. (2010). GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova). The European Journal of Neuroscience. Wiley-Blackwell. https://doi.org/10.1111/j.1460-9568.2010.07189.x","ieee":"P. M. Jonas and S. Hefft, “GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova),” The European Journal of Neuroscience, vol. 31, no. 7. Wiley-Blackwell, pp. 1194–1195, 2010."},"language":[{"iso":"eng"}],"doi":"10.1111/j.1460-9568.2010.07189.x","date_published":"2010-03-19T00:00:00Z","scopus_import":1,"day":"19","month":"03","article_processing_charge":"No","publication_status":"published","status":"public","title":"GABA release at terminals of CCK-interneurons: synchrony, asynchrony and modulation by cannabinoid receptors (commentary on Ali & Todorova)","department":[{"_id":"PeJo"}],"publisher":"Wiley-Blackwell","intvolume":" 31","_id":"3833","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","year":"2010","date_updated":"2021-01-12T07:52:31Z","date_created":"2018-12-11T12:05:25Z","volume":31,"oa_version":"None","author":[{"full_name":"Jonas, Peter M","last_name":"Jonas","first_name":"Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Hefft, Stefan","first_name":"Stefan","last_name":"Hefft"}],"type":"journal_article","publist_id":"2378","issue":"7"}]