[{"publication":"Science","citation":{"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.","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","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","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.","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.","short":"J. Guzmán, A. Schlögl, M. Frotscher, P.M. Jonas, Science 353 (2016) 1117–1123."},"page":"1117 - 1123","date_published":"2016-09-09T00:00:00Z","scopus_import":1,"day":"09","has_accepted_license":"1","_id":"1350","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","ddc":["570"],"status":"public","title":"Synaptic mechanisms of pattern completion in the hippocampal CA3 network","intvolume":" 353","pubrep_id":"823","file":[{"file_id":"4945","relation":"main_file","date_updated":"2020-07-14T12:44:46Z","date_created":"2018-12-12T10:12:27Z","checksum":"89caefa4e181424cbf0aecc835fcc5ec","file_name":"IST-2017-823-v1+1_aaf1836_CombinedPDF_v2-1.pdf","access_level":"open_access","creator":"system","file_size":19408143,"content_type":"application/pdf"}],"oa_version":"Preprint","type":"journal_article","abstract":[{"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.","lang":"eng"}],"issue":"6304","oa":1,"quality_controlled":"1","project":[{"call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","_id":"25C0F108-B435-11E9-9278-68D0E5697425","grant_number":"268548"},{"name":"Mechanisms of transmitter release at GABAergic synapses","call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","grant_number":"P24909-B24"}],"doi":"10.1126/science.aaf1836","acknowledged_ssus":[{"_id":"ScienComp"}],"language":[{"iso":"eng"}],"month":"09","year":"2016","publication_status":"published","publisher":"American Association for the Advancement of Science","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"author":[{"id":"30CC5506-F248-11E8-B48F-1D18A9856A87","first_name":"José","last_name":"Guzmán","full_name":"Guzmán, José"},{"full_name":"Schlögl, Alois","orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","last_name":"Schlögl","first_name":"Alois"},{"last_name":"Frotscher","first_name":"Michael","full_name":"Frotscher, Michael"},{"orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","first_name":"Peter M","full_name":"Jonas, Peter M"}],"date_updated":"2021-01-12T06:50:04Z","date_created":"2018-12-11T11:51:31Z","volume":353,"file_date_updated":"2020-07-14T12:44:46Z","publist_id":"5899","ec_funded":1},{"month":"01","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","article_number":"1207393","license":"https://creativecommons.org/licenses/by/4.0/","publist_id":"5762","file_date_updated":"2020-07-14T12:44:54Z","department":[{"_id":"PeJo"}],"publisher":"Hindawi Publishing Corporation","publication_status":"published","year":"2016","volume":2016,"date_created":"2018-12-11T11:52:00Z","date_updated":"2021-01-12T06:50:43Z","author":[{"first_name":"José","last_name":"Guzmán","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","full_name":"Guzmán, José"},{"first_name":"Zoltan","last_name":"Gerevich","full_name":"Gerevich, Zoltan"}],"scopus_import":1,"has_accepted_license":"1","day":"01","citation":{"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).","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.","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","ista":"Guzmán J, Gerevich Z. 2016. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. 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.","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"},"publication":"Neural Plasticity","date_published":"2016-01-01T00:00:00Z","type":"journal_article","abstract":[{"lang":"eng","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."}],"intvolume":" 2016","title":"P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction","status":"public","ddc":["570"],"_id":"1435","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa_version":"Published Version","file":[{"creator":"system","content_type":"application/pdf","file_size":1395180,"file_name":"IST-2016-580-v1+1_1207393.pdf","access_level":"open_access","date_created":"2018-12-12T10:09:17Z","date_updated":"2020-07-14T12:44:54Z","checksum":"8dc5c2f3d44d4775a6e7e3edb0d7a0da","file_id":"4740","relation":"main_file"}],"pubrep_id":"580"},{"type":"conference_abstract","file_date_updated":"2023-05-16T07:03:56Z","_id":"12903","year":"2016","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","ddc":["000"],"status":"public","title":"High performance computing at IST Austria: Modelling the human hippocampus","publication_status":"published","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"publisher":"VSC - Vienna Scientific Cluster","author":[{"full_name":"Schlögl, Alois","last_name":"Schlögl","first_name":"Alois","orcid":"0000-0002-5621-8100","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Stadlbauer, Stephan","id":"4D0BC184-F248-11E8-B48F-1D18A9856A87","first_name":"Stephan","last_name":"Stadlbauer"}],"date_created":"2023-05-05T12:54:47Z","date_updated":"2023-05-16T07:15:14Z","file":[{"access_level":"open_access","file_name":"2016_AHPC_Schloegl.pdf","creator":"dernst","content_type":"application/pdf","file_size":1073523,"file_id":"12968","relation":"main_file","success":1,"checksum":"4a7b00362e81358d568f5e216fa03c3e","date_created":"2023-05-16T07:03:56Z","date_updated":"2023-05-16T07:03:56Z"}],"oa_version":"Published Version","day":"24","month":"02","has_accepted_license":"1","article_processing_charge":"No","publication":"AHPC16 - Austrian HPC Meeting 2016","oa":1,"citation":{"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.","short":"A. Schlögl, S. Stadlbauer, in:, AHPC16 - Austrian HPC Meeting 2016, VSC - Vienna Scientific Cluster, 2016, p. 37.","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.","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.","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.","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.","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."},"main_file_link":[{"url":"https://vsc.ac.at/fileadmin/user_upload/vsc/conferences/ahpc16/BOOKLET_AHPC16.pdf","open_access":"1"}],"quality_controlled":"1","page":"37","conference":{"name":"AHPC: Austrian HPC Meeting","end_date":"2016-02-24","location":"Grundlsee, Austria","start_date":"2016-02-22"},"date_published":"2016-02-24T00:00:00Z","language":[{"iso":"eng"}]},{"intvolume":" 7","title":"Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks","status":"public","ddc":["570"],"_id":"1432","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","oa_version":"Published Version","file":[{"checksum":"7e84d0392348c874d473b62f1042de22","date_updated":"2020-07-14T12:44:53Z","date_created":"2018-12-12T10:18:33Z","file_id":"5355","relation":"main_file","creator":"system","file_size":4510512,"content_type":"application/pdf","access_level":"open_access","file_name":"IST-2016-582-v1+1_ncomms11552.pdf"}],"pubrep_id":"582","type":"journal_article","abstract":[{"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.","lang":"eng"}],"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.","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","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.","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"},"publication":"Nature Communications","date_published":"2016-05-13T00:00:00Z","scopus_import":1,"has_accepted_license":"1","day":"13","department":[{"_id":"PeJo"}],"publisher":"Nature Publishing Group","publication_status":"published","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. ","volume":7,"date_updated":"2023-09-07T11:55:25Z","date_created":"2018-12-11T11:51:59Z","related_material":{"record":[{"id":"1396","status":"public","relation":"dissertation_contains"}]},"author":[{"first_name":"Rajiv Kumar","last_name":"Mishra","id":"46CB58F2-F248-11E8-B48F-1D18A9856A87","full_name":"Mishra, Rajiv Kumar"},{"full_name":"Kim, Sooyun","first_name":"Sooyun","last_name":"Kim","id":"394AB1C8-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Guzmán, José","first_name":"José","last_name":"Guzmán","id":"30CC5506-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0003-2209-5242"},{"last_name":"Jonas","first_name":"Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M"}],"article_number":"11552","ec_funded":1,"publist_id":"5766","file_date_updated":"2020-07-14T12:44:53Z","project":[{"name":"Mechanisms of transmitter release at GABAergic synapses","call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","grant_number":"P24909-B24"},{"call_identifier":"FP7","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","grant_number":"268548","_id":"25C0F108-B435-11E9-9278-68D0E5697425"}],"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":"10.1038/ncomms11552","month":"05"},{"language":[{"iso":"eng"}],"degree_awarded":"PhD","supervisor":[{"first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"oa":1,"publication_identifier":{"issn":["2663-337X"]},"month":"03","related_material":{"record":[{"status":"public","relation":"part_of_dissertation","id":"1432"}]},"author":[{"full_name":"Mishra, Rajiv Kumar","id":"46CB58F2-F248-11E8-B48F-1D18A9856A87","first_name":"Rajiv Kumar","last_name":"Mishra"}],"date_updated":"2023-09-07T11:55:26Z","date_created":"2018-12-11T11:51:46Z","year":"2016","department":[{"_id":"PeJo"}],"publisher":"Institute of Science and Technology Austria","publication_status":"published","publist_id":"5811","file_date_updated":"2021-02-22T11:48:44Z","date_published":"2016-03-01T00:00:00Z","citation":{"short":"R.K. Mishra, Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus, Institute of Science and Technology Austria, 2016.","mla":"Mishra, Rajiv Kumar. 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.","apa":"Mishra, R. K. (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.","ista":"Mishra RK. 2016. Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus. Institute of Science and Technology Austria."},"page":"83","has_accepted_license":"1","article_processing_charge":"No","day":"01","file":[{"file_id":"6782","relation":"main_file","checksum":"5a010a838faf040f7064f3cfb802f743","date_created":"2019-08-09T12:14:46Z","date_updated":"2020-07-14T12:44:48Z","access_level":"closed","file_name":"Thesis_Mishra_Rajiv (Final).pdf","creator":"dernst","content_type":"application/pdf","file_size":2407572},{"creator":"dernst","content_type":"application/pdf","file_size":2407572,"file_name":"2016_RajivMishra_Thesis.pdf","access_level":"open_access","date_created":"2021-02-22T11:48:44Z","date_updated":"2021-02-22T11:48:44Z","success":1,"checksum":"81b26d9ede92c99f1d8cc6fa1d04cbbb","file_id":"9183","relation":"main_file"}],"oa_version":"Published Version","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","_id":"1396","ddc":["570"],"status":"public","title":"Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus","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."}],"type":"dissertation","alternative_title":["ISTA Thesis"]},{"author":[{"first_name":"Janina","last_name":"Kowalski","id":"3F3CA136-F248-11E8-B48F-1D18A9856A87","full_name":"Kowalski, Janina"},{"id":"3614E438-F248-11E8-B48F-1D18A9856A87","first_name":"Jian","last_name":"Gan","full_name":"Gan, Jian"},{"full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","first_name":"Peter M"},{"id":"36963E98-F248-11E8-B48F-1D18A9856A87","first_name":"Alejandro","last_name":"Pernia-Andrade","full_name":"Pernia-Andrade, Alejandro"}],"date_created":"2018-12-11T11:53:03Z","date_updated":"2023-10-17T10:02:02Z","volume":26,"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.","publication_status":"published","publisher":"Wiley","department":[{"_id":"PeJo"}],"file_date_updated":"2020-07-14T12:45:07Z","publist_id":"5550","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","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","month":"05","publication_identifier":{"issn":["1050-9631"],"eissn":["1098-1063"]},"pubrep_id":"469","file":[{"creator":"system","content_type":"application/pdf","file_size":905348,"file_name":"IST-2016-469-v1+1_Kowalski_et_al-Hippocampus.pdf","access_level":"open_access","date_updated":"2020-07-14T12:45:07Z","date_created":"2018-12-12T10:13:47Z","checksum":"284b72b12fbe15474833ed3d4549f86b","file_id":"5033","relation":"main_file"}],"oa_version":"Published Version","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1616","title":"Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats","status":"public","ddc":["570"],"intvolume":" 26","abstract":[{"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.","lang":"eng"}],"issue":"5","type":"journal_article","date_published":"2016-05-01T00:00:00Z","publication":"Hippocampus","citation":{"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.","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.","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","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","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.","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."},"page":"668 - 682","day":"01","has_accepted_license":"1","article_processing_charge":"No","scopus_import":"1"},{"article_processing_charge":"No","day":"01","scopus_import":1,"date_published":"2015-10-01T00:00:00Z","citation":{"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.","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.","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","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.","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.","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"},"publication":"Current Molecular Pharmacology","page":"149 - 161","article_type":"original","issue":"2","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"}],"type":"journal_article","oa_version":"Submitted Version","_id":"1535","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","intvolume":" 8","status":"public","title":"Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells","month":"10","doi":"10.2174/1874467208666150507105443","language":[{"iso":"eng"}],"oa":1,"external_id":{"pmid":["25966692"]},"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384372/"}],"quality_controlled":"1","publist_id":"5636","author":[{"orcid":"0000-0001-7577-1676","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","last_name":"Vandael","first_name":"David H","full_name":"Vandael, David H"},{"first_name":"Andrea","last_name":"Marcantoni","full_name":"Marcantoni, Andrea"},{"full_name":"Carbone, Emilio","last_name":"Carbone","first_name":"Emilio"}],"volume":8,"date_created":"2018-12-11T11:52:35Z","date_updated":"2021-01-12T06:51:26Z","pmid":1,"year":"2015","acknowledgement":"This work was supported by the Italian MIUR (PRIN 2010/2011 project 2010JFYFY2) and the University of Torino.","department":[{"_id":"PeJo"}],"publisher":"Bentham Science Publishers","publication_status":"published"},{"date_published":"2015-11-15T00:00:00Z","page":"4835 - 4853","citation":{"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.","short":"D. Gavello, D.H. Vandael, S. Gosso, E. Carbone, V. Carabelli, Journal of Physiology 593 (2015) 4835–4853.","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.","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","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.","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"},"publication":"Journal of Physiology","day":"15","scopus_import":1,"oa_version":"Submitted Version","intvolume":" 593","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","_id":"1565","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","issue":"22","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"}],"type":"journal_article","language":[{"iso":"eng"}],"doi":"10.1113/JP271078","quality_controlled":"1","oa":1,"external_id":{"pmid":["26282459"]},"main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650409/"}],"month":"11","volume":593,"date_created":"2018-12-11T11:52:45Z","date_updated":"2021-01-12T06:51:38Z","author":[{"last_name":"Gavello","first_name":"Daniela","full_name":"Gavello, Daniela"},{"first_name":"David H","last_name":"Vandael","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7577-1676","full_name":"Vandael, David H"},{"last_name":"Gosso","first_name":"Sara","full_name":"Gosso, Sara"},{"full_name":"Carbone, Emilio","last_name":"Carbone","first_name":"Emilio"},{"full_name":"Carabelli, Valentina","last_name":"Carabelli","first_name":"Valentina"}],"publisher":"Wiley-Blackwell","department":[{"_id":"PeJo"}],"publication_status":"published","pmid":1,"year":"2015","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.","publist_id":"5606"},{"_id":"1580","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","title":"Knock-down of synapsin alters cell excitability and action potential waveform by potentiating BK and voltage gated Ca2 currents in Helix serotonergic neurons","status":"public","ddc":["570"],"intvolume":" 311","file":[{"relation":"main_file","file_id":"7849","date_created":"2020-05-15T06:50:20Z","date_updated":"2020-07-14T12:45:02Z","checksum":"af2c4c994718c7be417eba0dc746aac9","file_name":"2015_Neuroscience_Brenes.pdf","access_level":"open_access","content_type":"application/pdf","file_size":5563015,"creator":"dernst"}],"oa_version":"Submitted Version","type":"journal_article","abstract":[{"lang":"eng","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."}],"publication":"Neuroscience","citation":{"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","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.","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.","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."},"article_type":"original","page":"430 - 443","date_published":"2015-12-17T00:00:00Z","scopus_import":1,"day":"17","has_accepted_license":"1","article_processing_charge":"No","year":"2015","publication_status":"published","publisher":"Elsevier","department":[{"_id":"PeJo"}],"author":[{"last_name":"Brenes","first_name":"Oscar","full_name":"Brenes, Oscar"},{"full_name":"Vandael, David H","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7577-1676","first_name":"David H","last_name":"Vandael"},{"last_name":"Carbone","first_name":"Emilio","full_name":"Carbone, Emilio"},{"full_name":"Montarolo, Pier","last_name":"Montarolo","first_name":"Pier"},{"first_name":"Mirella","last_name":"Ghirardi","full_name":"Ghirardi, Mirella"}],"date_updated":"2021-01-12T06:51:44Z","date_created":"2018-12-11T11:52:50Z","volume":311,"file_date_updated":"2020-07-14T12:45:02Z","publist_id":"5591","oa":1,"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"},"quality_controlled":"1","doi":"10.1016/j.neuroscience.2015.10.046","language":[{"iso":"eng"}],"month":"12"},{"pubrep_id":"470","file":[{"access_level":"open_access","file_name":"IST-2016-470-v1+1_1-s2.0-S2211124715010220-main.pdf","creator":"system","file_size":2314406,"content_type":"application/pdf","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","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","_id":"1615","ddc":["570"],"status":"public","title":"Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism","intvolume":" 13","abstract":[{"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.","lang":"eng"}],"issue":"3","type":"journal_article","date_published":"2015-10-20T00:00:00Z","publication":"Cell Reports","citation":{"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.","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"},"page":"516 - 523","day":"20","has_accepted_license":"1","scopus_import":1,"author":[{"last_name":"Hammer","first_name":"Matthieu","full_name":"Hammer, Matthieu"},{"full_name":"Krueger Burg, Dilja","last_name":"Krueger Burg","first_name":"Dilja"},{"first_name":"Liam","last_name":"Tuffy","full_name":"Tuffy, Liam"},{"last_name":"Cooper","first_name":"Benjamin","full_name":"Cooper, Benjamin"},{"full_name":"Taschenberger, Holger","first_name":"Holger","last_name":"Taschenberger"},{"full_name":"Goswami, Sarit","id":"3A578F32-F248-11E8-B48F-1D18A9856A87","first_name":"Sarit","last_name":"Goswami"},{"last_name":"Ehrenreich","first_name":"Hannelore","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"},{"last_name":"Varoqueaux","first_name":"Frederique","full_name":"Varoqueaux, Frederique"},{"last_name":"Rhee","first_name":"Jeong","full_name":"Rhee, Jeong"},{"full_name":"Brose, Nils","first_name":"Nils","last_name":"Brose"}],"date_updated":"2021-01-12T06:52:01Z","date_created":"2018-12-11T11:53:02Z","volume":13,"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.","publication_status":"published","publisher":"Cell Press","department":[{"_id":"PeJo"}],"file_date_updated":"2020-07-14T12:45:07Z","publist_id":"5551","doi":"10.1016/j.celrep.2015.09.011","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","month":"10"}]