--- _id: '1350' 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." acknowledged_ssus: - _id: ScienComp author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Michael full_name: Frotscher, Michael last_name: Frotscher - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: 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 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 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. 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. 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. 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. date_created: 2018-12-11T11:51:31Z date_published: 2016-09-09T00:00:00Z date_updated: 2021-01-12T06:50:04Z day: '09' ddc: - '570' department: - _id: ScienComp - _id: PeJo doi: 10.1126/science.aaf1836 ec_funded: 1 file: - access_level: open_access checksum: 89caefa4e181424cbf0aecc835fcc5ec content_type: application/pdf creator: system date_created: 2018-12-12T10:12:27Z date_updated: 2020-07-14T12:44:46Z file_id: '4945' file_name: IST-2017-823-v1+1_aaf1836_CombinedPDF_v2-1.pdf file_size: 19408143 relation: main_file file_date_updated: 2020-07-14T12:44:46Z has_accepted_license: '1' intvolume: ' 353' issue: '6304' language: - iso: eng month: '09' oa: 1 oa_version: Preprint page: 1117 - 1123 project: - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5899' pubrep_id: '823' quality_controlled: '1' scopus_import: 1 status: public title: Synaptic mechanisms of pattern completion in the hippocampal CA3 network type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 353 year: '2016' ... --- _id: '1435' 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. article_number: '1207393' author: - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán - first_name: Zoltan full_name: Gerevich, Zoltan last_name: Gerevich citation: 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' 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' 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.' 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.' ista: 'Guzmán J, Gerevich Z. 2016. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. 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). date_created: 2018-12-11T11:52:00Z date_published: 2016-01-01T00:00:00Z date_updated: 2021-01-12T06:50:43Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1155/2016/1207393 file: - access_level: open_access checksum: 8dc5c2f3d44d4775a6e7e3edb0d7a0da content_type: application/pdf creator: system date_created: 2018-12-12T10:09:17Z date_updated: 2020-07-14T12:44:54Z file_id: '4740' file_name: IST-2016-580-v1+1_1207393.pdf file_size: 1395180 relation: main_file file_date_updated: 2020-07-14T12:44:54Z has_accepted_license: '1' intvolume: ' 2016' language: - iso: eng month: '01' oa: 1 oa_version: Published Version publication: Neural Plasticity publication_status: published publisher: Hindawi Publishing Corporation publist_id: '5762' pubrep_id: '580' quality_controlled: '1' scopus_import: 1 status: public title: 'P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 2016 year: '2016' ... --- _id: '12903' article_processing_charge: No author: - first_name: Alois full_name: Schlögl, Alois id: 45BF87EE-F248-11E8-B48F-1D18A9856A87 last_name: Schlögl orcid: 0000-0002-5621-8100 - first_name: Stephan full_name: Stadlbauer, Stephan id: 4D0BC184-F248-11E8-B48F-1D18A9856A87 last_name: Stadlbauer citation: 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.' 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.' 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.' 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.' 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.' 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. conference: end_date: 2016-02-24 location: Grundlsee, Austria name: 'AHPC: Austrian HPC Meeting' start_date: 2016-02-22 date_created: 2023-05-05T12:54:47Z date_published: 2016-02-24T00:00:00Z date_updated: 2023-05-16T07:15:14Z day: '24' ddc: - '000' department: - _id: ScienComp - _id: PeJo file: - access_level: open_access checksum: 4a7b00362e81358d568f5e216fa03c3e content_type: application/pdf creator: dernst date_created: 2023-05-16T07:03:56Z date_updated: 2023-05-16T07:03:56Z file_id: '12968' file_name: 2016_AHPC_Schloegl.pdf file_size: 1073523 relation: main_file success: 1 file_date_updated: 2023-05-16T07:03:56Z has_accepted_license: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://vsc.ac.at/fileadmin/user_upload/vsc/conferences/ahpc16/BOOKLET_AHPC16.pdf month: '02' oa: 1 oa_version: Published Version page: '37' publication: AHPC16 - Austrian HPC Meeting 2016 publication_status: published publisher: VSC - Vienna Scientific Cluster quality_controlled: '1' status: public title: 'High performance computing at IST Austria: Modelling the human hippocampus' type: conference_abstract user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2016' ... --- _id: '1432' 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. 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. ' article_number: '11552' author: - first_name: Rajiv Kumar full_name: Mishra, Rajiv Kumar id: 46CB58F2-F248-11E8-B48F-1D18A9856A87 last_name: Mishra - first_name: Sooyun full_name: Kim, Sooyun id: 394AB1C8-F248-11E8-B48F-1D18A9856A87 last_name: Kim - first_name: José full_name: Guzmán, José id: 30CC5506-F248-11E8-B48F-1D18A9856A87 last_name: Guzmán orcid: 0000-0003-2209-5242 - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 citation: 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 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 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. 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. 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. 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). date_created: 2018-12-11T11:51:59Z date_published: 2016-05-13T00:00:00Z date_updated: 2023-09-07T11:55:25Z day: '13' ddc: - '570' department: - _id: PeJo doi: 10.1038/ncomms11552 ec_funded: 1 file: - access_level: open_access checksum: 7e84d0392348c874d473b62f1042de22 content_type: application/pdf creator: system date_created: 2018-12-12T10:18:33Z date_updated: 2020-07-14T12:44:53Z file_id: '5355' file_name: IST-2016-582-v1+1_ncomms11552.pdf file_size: 4510512 relation: main_file file_date_updated: 2020-07-14T12:44:53Z has_accepted_license: '1' intvolume: ' 7' language: - iso: eng month: '05' oa: 1 oa_version: Published Version project: - _id: 25C26B1E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P24909-B24 name: Mechanisms of transmitter release at GABAergic synapses - _id: 25C0F108-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '268548' name: Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons publication: Nature Communications publication_status: published publisher: Nature Publishing Group publist_id: '5766' pubrep_id: '582' quality_controlled: '1' related_material: record: - id: '1396' relation: dissertation_contains status: public scopus_import: 1 status: public title: Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 7 year: '2016' ... --- _id: '1396' 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. alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Rajiv Kumar full_name: Mishra, Rajiv Kumar id: 46CB58F2-F248-11E8-B48F-1D18A9856A87 last_name: Mishra citation: 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. chicago: Mishra, Rajiv Kumar. “Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus.” Institute of Science and Technology Austria, 2016. 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. 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. date_created: 2018-12-11T11:51:46Z date_published: 2016-03-01T00:00:00Z date_updated: 2023-09-07T11:55:26Z day: '01' ddc: - '570' degree_awarded: PhD department: - _id: PeJo file: - access_level: closed checksum: 5a010a838faf040f7064f3cfb802f743 content_type: application/pdf creator: dernst date_created: 2019-08-09T12:14:46Z date_updated: 2020-07-14T12:44:48Z file_id: '6782' file_name: Thesis_Mishra_Rajiv (Final).pdf file_size: 2407572 relation: main_file - access_level: open_access checksum: 81b26d9ede92c99f1d8cc6fa1d04cbbb content_type: application/pdf creator: dernst date_created: 2021-02-22T11:48:44Z date_updated: 2021-02-22T11:48:44Z file_id: '9183' file_name: 2016_RajivMishra_Thesis.pdf file_size: 2407572 relation: main_file success: 1 file_date_updated: 2021-02-22T11:48:44Z has_accepted_license: '1' language: - iso: eng month: '03' oa: 1 oa_version: Published Version page: '83' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '5811' related_material: record: - id: '1432' relation: part_of_dissertation status: public status: public supervisor: - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 title: Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2016' ... --- _id: '1616' 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. acknowledgement: "The authors thank Jose Guzman 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." article_processing_charge: No author: - first_name: Janina full_name: Kowalski, Janina id: 3F3CA136-F248-11E8-B48F-1D18A9856A87 last_name: Kowalski - first_name: Jian full_name: Gan, Jian id: 3614E438-F248-11E8-B48F-1D18A9856A87 last_name: Gan - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Alejandro full_name: Pernia-Andrade, Alejandro id: 36963E98-F248-11E8-B48F-1D18A9856A87 last_name: Pernia-Andrade citation: 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 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. 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. 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. short: J. Kowalski, J. Gan, P.M. Jonas, A. Pernia-Andrade, Hippocampus 26 (2016) 668–682. date_created: 2018-12-11T11:53:03Z date_published: 2016-05-01T00:00:00Z date_updated: 2023-10-17T10:02:02Z day: '01' ddc: - '570' department: - _id: PeJo doi: 10.1002/hipo.22550 file: - access_level: open_access checksum: 284b72b12fbe15474833ed3d4549f86b content_type: application/pdf creator: system date_created: 2018-12-12T10:13:47Z date_updated: 2020-07-14T12:45:07Z file_id: '5033' file_name: IST-2016-469-v1+1_Kowalski_et_al-Hippocampus.pdf file_size: 905348 relation: main_file file_date_updated: 2020-07-14T12:45:07Z has_accepted_license: '1' intvolume: ' 26' issue: '5' language: - iso: eng month: '05' oa: 1 oa_version: Published Version page: 668 - 682 publication: Hippocampus publication_identifier: eissn: - 1098-1063 issn: - 1050-9631 publication_status: published publisher: Wiley publist_id: '5550' pubrep_id: '469' quality_controlled: '1' scopus_import: '1' status: public title: Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 26 year: '2016' ... --- _id: '1535' abstract: - lang: eng 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. acknowledgement: This work was supported by the Italian MIUR (PRIN 2010/2011 project 2010JFYFY2) and the University of Torino. article_processing_charge: No article_type: original author: - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: Andrea full_name: Marcantoni, Andrea last_name: Marcantoni - first_name: Emilio full_name: Carbone, Emilio last_name: Carbone citation: 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 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 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. 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. 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. 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. date_created: 2018-12-11T11:52:35Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:51:26Z day: '01' department: - _id: PeJo doi: 10.2174/1874467208666150507105443 external_id: pmid: - '25966692' intvolume: ' 8' issue: '2' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384372/ month: '10' oa: 1 oa_version: Submitted Version page: 149 - 161 pmid: 1 publication: Current Molecular Pharmacology publication_status: published publisher: Bentham Science Publishers publist_id: '5636' quality_controlled: '1' scopus_import: 1 status: public title: Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2015' ... --- _id: '1565' abstract: - lang: eng 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. 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." author: - first_name: Daniela full_name: Gavello, Daniela last_name: Gavello - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: Sara full_name: Gosso, Sara last_name: Gosso - first_name: Emilio full_name: Carbone, Emilio last_name: Carbone - first_name: Valentina full_name: Carabelli, Valentina last_name: Carabelli citation: 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 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 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. 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. 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. 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. date_created: 2018-12-11T11:52:45Z date_published: 2015-11-15T00:00:00Z date_updated: 2021-01-12T06:51:38Z day: '15' department: - _id: PeJo doi: 10.1113/JP271078 external_id: pmid: - '26282459' intvolume: ' 593' issue: '22' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650409/ month: '11' oa: 1 oa_version: Submitted Version page: 4835 - 4853 pmid: 1 publication: Journal of Physiology publication_status: published publisher: Wiley-Blackwell publist_id: '5606' quality_controlled: '1' scopus_import: 1 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 type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 593 year: '2015' ... --- _id: '1580' 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. article_processing_charge: No article_type: original author: - first_name: Oscar full_name: Brenes, Oscar last_name: Brenes - first_name: David H full_name: Vandael, David H id: 3AE48E0A-F248-11E8-B48F-1D18A9856A87 last_name: Vandael orcid: 0000-0001-7577-1676 - first_name: Emilio full_name: Carbone, Emilio last_name: Carbone - first_name: Pier full_name: Montarolo, Pier last_name: Montarolo - first_name: Mirella full_name: Ghirardi, Mirella last_name: Ghirardi 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 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 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. 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. 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. 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. short: O. Brenes, D.H. Vandael, E. Carbone, P. Montarolo, M. Ghirardi, Neuroscience 311 (2015) 430–443. date_created: 2018-12-11T11:52:50Z date_published: 2015-12-17T00:00:00Z date_updated: 2021-01-12T06:51:44Z day: '17' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.neuroscience.2015.10.046 file: - access_level: open_access checksum: af2c4c994718c7be417eba0dc746aac9 content_type: application/pdf creator: dernst date_created: 2020-05-15T06:50:20Z date_updated: 2020-07-14T12:45:02Z file_id: '7849' file_name: 2015_Neuroscience_Brenes.pdf file_size: 5563015 relation: main_file file_date_updated: 2020-07-14T12:45:02Z has_accepted_license: '1' intvolume: ' 311' language: - iso: eng month: '12' oa: 1 oa_version: Submitted Version page: 430 - 443 publication: Neuroscience publication_status: published publisher: Elsevier publist_id: '5591' quality_controlled: '1' scopus_import: 1 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 tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 311 year: '2015' ... --- _id: '1615' 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. 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. author: - first_name: Matthieu full_name: Hammer, Matthieu last_name: Hammer - first_name: Dilja full_name: Krueger Burg, Dilja last_name: Krueger Burg - first_name: Liam full_name: Tuffy, Liam last_name: Tuffy - first_name: Benjamin full_name: Cooper, Benjamin last_name: Cooper - first_name: Holger full_name: Taschenberger, Holger last_name: Taschenberger - first_name: Sarit full_name: Goswami, Sarit id: 3A578F32-F248-11E8-B48F-1D18A9856A87 last_name: Goswami - first_name: Hannelore full_name: Ehrenreich, Hannelore last_name: Ehrenreich - first_name: Peter M full_name: Jonas, Peter M id: 353C1B58-F248-11E8-B48F-1D18A9856A87 last_name: Jonas orcid: 0000-0001-5001-4804 - first_name: Frederique full_name: Varoqueaux, Frederique last_name: Varoqueaux - first_name: Jeong full_name: Rhee, Jeong last_name: Rhee - first_name: Nils full_name: Brose, Nils last_name: Brose citation: 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 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 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. 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. 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. 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. date_created: 2018-12-11T11:53:02Z date_published: 2015-10-20T00:00:00Z date_updated: 2021-01-12T06:52:01Z day: '20' ddc: - '570' department: - _id: PeJo doi: 10.1016/j.celrep.2015.09.011 file: - access_level: open_access checksum: 44d30fbb543774b076b4938bd36af9d7 content_type: application/pdf creator: system date_created: 2018-12-12T10:13:23Z date_updated: 2020-07-14T12:45:07Z file_id: '5005' file_name: IST-2016-470-v1+1_1-s2.0-S2211124715010220-main.pdf file_size: 2314406 relation: main_file file_date_updated: 2020-07-14T12:45:07Z has_accepted_license: '1' intvolume: ' 13' issue: '3' language: - iso: eng month: '10' oa: 1 oa_version: Published Version page: 516 - 523 publication: Cell Reports publication_status: published publisher: Cell Press publist_id: '5551' pubrep_id: '470' quality_controlled: '1' scopus_import: 1 status: public title: Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 13 year: '2015' ...