[{"user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"MiSi"},{"_id":"PeJo"}],"title":"Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions","status":"public","publisher":"Nature Publishing Group","acknowledgement":"Y. Fukui (Medical Institute of Bioregulation, Kyushu University) and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children's Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct. pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding retrovirus was kindly provided by A. Leithner (Institute of Science and Technology Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research, National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent technical support (Core imaging facility, Medical University of Vienna). We thank D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was supported by the Austrian Academy of Sciences, the Science Fund of the Austrian National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA framework (to S.Knapp).","publist_id":"6216","publication":"Nature Immunology","main_file_link":[{"open_access":"1","url":"https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d"}],"oa_version":"Submitted Version","page":"1361 - 1372","volume":17,"quality_controlled":"1","oa":1,"citation":{"short":"R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo, F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau, A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer, J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372.","chicago":"Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” <i>Nature Immunology</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/ni.3590\">https://doi.org/10.1038/ni.3590</a>.","ieee":"R. Martins <i>et al.</i>, “Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions,” <i>Nature Immunology</i>, vol. 17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016.","apa":"Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp, S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. <i>Nature Immunology</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ni.3590\">https://doi.org/10.1038/ni.3590</a>","ama":"Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. <i>Nature Immunology</i>. 2016;17(12):1361-1372. doi:<a href=\"https://doi.org/10.1038/ni.3590\">10.1038/ni.3590</a>","mla":"Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” <i>Nature Immunology</i>, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1361–72, doi:<a href=\"https://doi.org/10.1038/ni.3590\">10.1038/ni.3590</a>.","ista":"Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 17(12), 1361–1372."},"day":"01","publication_status":"published","intvolume":"        17","type":"journal_article","date_updated":"2021-01-12T06:48:36Z","doi":"10.1038/ni.3590","year":"2016","language":[{"iso":"eng"}],"month":"12","date_published":"2016-12-01T00:00:00Z","scopus_import":1,"_id":"1142","date_created":"2018-12-11T11:50:22Z","issue":"12","author":[{"first_name":"Rui","last_name":"Martins","full_name":"Martins, Rui"},{"full_name":"Maier, Julia","last_name":"Maier","first_name":"Julia"},{"full_name":"Gorki, Anna","last_name":"Gorki","first_name":"Anna"},{"last_name":"Huber","first_name":"Kilian","full_name":"Huber, Kilian"},{"full_name":"Sharif, Omar","first_name":"Omar","last_name":"Sharif"},{"last_name":"Starkl","first_name":"Philipp","full_name":"Starkl, Philipp"},{"full_name":"Saluzzo, Simona","last_name":"Saluzzo","first_name":"Simona"},{"full_name":"Quattrone, Federica","first_name":"Federica","last_name":"Quattrone"},{"full_name":"Gawish, Riem","first_name":"Riem","last_name":"Gawish"},{"last_name":"Lakovits","first_name":"Karin","full_name":"Lakovits, Karin"},{"first_name":"Michael","last_name":"Aichinger","full_name":"Aichinger, Michael"},{"full_name":"Radic Sarikas, Branka","first_name":"Branka","last_name":"Radic Sarikas"},{"full_name":"Lardeau, Charles","last_name":"Lardeau","first_name":"Charles"},{"first_name":"Anastasiya","last_name":"Hladik","full_name":"Hladik, Anastasiya"},{"full_name":"Korosec, Ana","first_name":"Ana","last_name":"Korosec"},{"id":"3DAB9AFC-F248-11E8-B48F-1D18A9856A87","first_name":"Markus","last_name":"Brown","full_name":"Brown, Markus"},{"id":"368EE576-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7829-3518","last_name":"Vaahtomeri","first_name":"Kari","full_name":"Vaahtomeri, Kari"},{"full_name":"Duggan, Michelle","first_name":"Michelle","last_name":"Duggan","id":"2EDEA62C-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Kerjaschki","first_name":"Dontscho","full_name":"Kerjaschki, Dontscho"},{"full_name":"Esterbauer, Harald","last_name":"Esterbauer","first_name":"Harald"},{"full_name":"Colinge, Jacques","last_name":"Colinge","first_name":"Jacques"},{"full_name":"Eisenbarth, Stephanie","last_name":"Eisenbarth","first_name":"Stephanie"},{"full_name":"Decker, Thomas","first_name":"Thomas","last_name":"Decker"},{"full_name":"Bennett, Keiryn","last_name":"Bennett","first_name":"Keiryn"},{"full_name":"Kubicek, Stefan","last_name":"Kubicek","first_name":"Stefan"},{"full_name":"Sixt, Michael K","last_name":"Sixt","orcid":"0000-0002-6620-9179","first_name":"Michael K","id":"41E9FBEA-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Superti Furga, Giulio","first_name":"Giulio","last_name":"Superti Furga"},{"full_name":"Knapp, Sylvia","last_name":"Knapp","first_name":"Sylvia"}],"abstract":[{"text":"Hemolysis drives susceptibility to bacterial infections and predicts poor outcome from sepsis. These detrimental effects are commonly considered to be a consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative sepsis model and found that elevated heme levels impaired the control of bacterial proliferation independently of heme-iron acquisition by pathogens. Heme strongly inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach revealed that quinine effectively prevented heme effects on the cytoskeleton, restored phagocytosis and improved survival in sepsis. These mechanistic insights provide potential therapeutic targets for patients with sepsis or hemolytic disorders.","lang":"eng"}]},{"issue":"5","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"}],"author":[{"last_name":"Kowalski","first_name":"Janina","full_name":"Kowalski, Janina","id":"3F3CA136-F248-11E8-B48F-1D18A9856A87"},{"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","last_name":"Jonas","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"id":"36963E98-F248-11E8-B48F-1D18A9856A87","full_name":"Pernia-Andrade, Alejandro","first_name":"Alejandro","last_name":"Pernia-Andrade"}],"pubrep_id":"469","license":"https://creativecommons.org/licenses/by-nc-nd/4.0/","date_published":"2016-05-01T00:00:00Z","scopus_import":"1","_id":"1616","date_created":"2018-12-11T11:53:03Z","ddc":["570"],"doi":"10.1002/hipo.22550","year":"2016","language":[{"iso":"eng"}],"month":"05","publication_status":"published","intvolume":"        26","type":"journal_article","date_updated":"2023-10-17T10:02:02Z","publication_identifier":{"issn":["1050-9631"],"eissn":["1098-1063"]},"quality_controlled":"1","oa":1,"citation":{"short":"J. Kowalski, J. Gan, P.M. Jonas, A. Pernia-Andrade, Hippocampus 26 (2016) 668–682.","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,” <i>Hippocampus</i>, vol. 26, no. 5. Wiley, pp. 668–682, 2016.","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.” <i>Hippocampus</i>. Wiley, 2016. <a href=\"https://doi.org/10.1002/hipo.22550\">https://doi.org/10.1002/hipo.22550</a>.","apa":"Kowalski, J., Gan, J., Jonas, P. M., &#38; Pernia-Andrade, A. (2016). Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. <i>Hippocampus</i>. Wiley. <a href=\"https://doi.org/10.1002/hipo.22550\">https://doi.org/10.1002/hipo.22550</a>","mla":"Kowalski, Janina, et al. “Intrinsic Membrane Properties Determine Hippocampal Differential Firing Pattern in Vivo in Anesthetized Rats.” <i>Hippocampus</i>, vol. 26, no. 5, Wiley, 2016, pp. 668–82, doi:<a href=\"https://doi.org/10.1002/hipo.22550\">10.1002/hipo.22550</a>.","ama":"Kowalski J, Gan J, Jonas PM, Pernia-Andrade A. Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats. <i>Hippocampus</i>. 2016;26(5):668-682. doi:<a href=\"https://doi.org/10.1002/hipo.22550\">10.1002/hipo.22550</a>","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."},"day":"01","tmp":{"short":"CC BY-NC-ND (4.0)","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)","image":"/images/cc_by_nc_nd.png"},"page":"668 - 682","oa_version":"Published Version","volume":26,"file":[{"file_size":905348,"content_type":"application/pdf","relation":"main_file","file_name":"IST-2016-469-v1+1_Kowalski_et_al-Hippocampus.pdf","file_id":"5033","creator":"system","date_created":"2018-12-12T10:13:47Z","date_updated":"2020-07-14T12:45:07Z","access_level":"open_access","checksum":"284b72b12fbe15474833ed3d4549f86b"}],"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.","publist_id":"5550","article_processing_charge":"No","publication":"Hippocampus","file_date_updated":"2020-07-14T12:45:07Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","has_accepted_license":"1","title":"Intrinsic membrane properties determine hippocampal differential firing pattern in vivo in anesthetized rats","department":[{"_id":"PeJo"}],"status":"public","publisher":"Wiley"},{"article_number":"11552","day":"13","oa":1,"citation":{"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,” <i>Nature Communications</i>, vol. 7. Nature Publishing Group, 2016.","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.” <i>Nature Communications</i>. Nature Publishing Group, 2016. <a href=\"https://doi.org/10.1038/ncomms11552\">https://doi.org/10.1038/ncomms11552</a>.","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.","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. <i>Nature Communications</i>. 2016;7. doi:<a href=\"https://doi.org/10.1038/ncomms11552\">10.1038/ncomms11552</a>","mla":"Mishra, Rajiv Kumar, et al. “Symmetric Spike Timing-Dependent Plasticity at CA3–CA3 Synapses Optimizes Storage and Recall in Autoassociative Networks.” <i>Nature Communications</i>, vol. 7, 11552, Nature Publishing Group, 2016, doi:<a href=\"https://doi.org/10.1038/ncomms11552\">10.1038/ncomms11552</a>.","apa":"Mishra, R. K., Kim, S., Guzmán, J., &#38; Jonas, P. M. (2016). Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks. <i>Nature Communications</i>. Nature Publishing Group. <a href=\"https://doi.org/10.1038/ncomms11552\">https://doi.org/10.1038/ncomms11552</a>"},"quality_controlled":"1","file":[{"relation":"main_file","content_type":"application/pdf","file_name":"IST-2016-582-v1+1_ncomms11552.pdf","file_id":"5355","creator":"system","file_size":4510512,"checksum":"7e84d0392348c874d473b62f1042de22","access_level":"open_access","date_created":"2018-12-12T10:18:33Z","date_updated":"2020-07-14T12:44:53Z"}],"volume":7,"oa_version":"Published Version","tmp":{"image":"/images/cc_by.png","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)"},"publication":"Nature Communications","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. ","publist_id":"5766","project":[{"name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"},{"name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","_id":"25C0F108-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"268548"}],"publisher":"Nature Publishing Group","has_accepted_license":"1","department":[{"_id":"PeJo"}],"title":"Symmetric spike timing-dependent plasticity at CA3–CA3 synapses optimizes storage and recall in autoassociative networks","status":"public","file_date_updated":"2020-07-14T12:44:53Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","pubrep_id":"582","related_material":{"record":[{"relation":"dissertation_contains","status":"public","id":"1396"}]},"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."}],"ec_funded":1,"author":[{"full_name":"Mishra, Rajiv Kumar","first_name":"Rajiv Kumar","last_name":"Mishra","id":"46CB58F2-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Kim","first_name":"Sooyun","full_name":"Kim, Sooyun","id":"394AB1C8-F248-11E8-B48F-1D18A9856A87"},{"id":"30CC5506-F248-11E8-B48F-1D18A9856A87","first_name":"José","last_name":"Guzmán","orcid":"0000-0003-2209-5242","full_name":"Guzmán, José"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","first_name":"Peter M"}],"date_created":"2018-12-11T11:51:59Z","_id":"1432","date_published":"2016-05-13T00:00:00Z","scopus_import":1,"license":"https://creativecommons.org/licenses/by/4.0/","month":"05","language":[{"iso":"eng"}],"doi":"10.1038/ncomms11552","year":"2016","ddc":["570"],"type":"journal_article","date_updated":"2023-09-07T11:55:25Z","publication_status":"published","intvolume":"         7"},{"year":"2016","doi":"10.1155/2016/1207393","ddc":["570"],"month":"01","language":[{"iso":"eng"}],"intvolume":"      2016","publication_status":"published","date_updated":"2021-01-12T06:50:43Z","type":"journal_article","author":[{"id":"30CC5506-F248-11E8-B48F-1D18A9856A87","full_name":"Guzmán, José","first_name":"José","last_name":"Guzmán"},{"full_name":"Gerevich, Zoltan","first_name":"Zoltan","last_name":"Gerevich"}],"abstract":[{"text":"ATP released from neurons and astrocytes during neuronal activity or under pathophysiological circumstances is able to influence information flow in neuronal circuits by activation of ionotropic P2X and metabotropic P2Y receptors and subsequent modulation of cellular excitability, synaptic strength, and plasticity. In the present paper we review cellular and network effects of P2Y receptors in the brain. We show that P2Y receptors inhibit the release of neurotransmitters, modulate voltage- and ligand-gated ion channels, and differentially influence the induction of synaptic plasticity in the prefrontal cortex, hippocampus, and cerebellum. The findings discussed here may explain how P2Y1 receptor activation during brain injury, hypoxia, inflammation, schizophrenia, or Alzheimer's disease leads to an impairment of cognitive processes. Hence, it is suggested that the blockade of P2Y1 receptors may have therapeutic potential against cognitive disturbances in these states.","lang":"eng"}],"pubrep_id":"580","scopus_import":1,"date_published":"2016-01-01T00:00:00Z","date_created":"2018-12-11T11:52:00Z","_id":"1435","publist_id":"5762","publication":"Neural Plasticity","title":"P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction","status":"public","department":[{"_id":"PeJo"}],"has_accepted_license":"1","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","file_date_updated":"2020-07-14T12:44:54Z","publisher":"Hindawi Publishing Corporation","quality_controlled":"1","day":"01","article_number":"1207393","citation":{"apa":"Guzmán, J., &#38; Gerevich, Z. (2016). P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. <i>Neural Plasticity</i>. Hindawi Publishing Corporation. <a href=\"https://doi.org/10.1155/2016/1207393\">https://doi.org/10.1155/2016/1207393</a>","ama":"Guzmán J, Gerevich Z. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. <i>Neural Plasticity</i>. 2016;2016. doi:<a href=\"https://doi.org/10.1155/2016/1207393\">10.1155/2016/1207393</a>","mla":"Guzmán, José, and Zoltan Gerevich. “P2Y Receptors in Synaptic Transmission and Plasticity: Therapeutic Potential in Cognitive Dysfunction.” <i>Neural Plasticity</i>, vol. 2016, 1207393, Hindawi Publishing Corporation, 2016, doi:<a href=\"https://doi.org/10.1155/2016/1207393\">10.1155/2016/1207393</a>.","ista":"Guzmán J, Gerevich Z. 2016. P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction. Neural Plasticity. 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.” <i>Neural Plasticity</i>. Hindawi Publishing Corporation, 2016. <a href=\"https://doi.org/10.1155/2016/1207393\">https://doi.org/10.1155/2016/1207393</a>.","ieee":"J. Guzmán and Z. Gerevich, “P2Y receptors in synaptic transmission and plasticity: Therapeutic potential in cognitive dysfunction,” <i>Neural Plasticity</i>, vol. 2016. Hindawi Publishing Corporation, 2016."},"oa":1,"tmp":{"image":"/images/cc_by.png","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)"},"file":[{"date_created":"2018-12-12T10:09:17Z","date_updated":"2020-07-14T12:44:54Z","checksum":"8dc5c2f3d44d4775a6e7e3edb0d7a0da","access_level":"open_access","file_size":1395180,"file_name":"IST-2016-580-v1+1_1207393.pdf","content_type":"application/pdf","relation":"main_file","file_id":"4740","creator":"system"}],"volume":2016,"oa_version":"Published Version"},{"volume":5,"oa_version":"Published Version","file":[{"content_type":"application/pdf","relation":"main_file","file_name":"IST-2016-715-v1+1_e17977-download.pdf","creator":"system","file_id":"5257","file_size":1477891,"access_level":"open_access","checksum":"a7201280c571bed88ebd459ce5ce6a47","date_created":"2018-12-12T10:17:05Z","date_updated":"2020-07-14T12:44:44Z"}],"tmp":{"image":"/images/cc_by.png","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)"},"oa":1,"citation":{"short":"N. Vyleta, C. Borges Merjane, P.M. Jonas, ELife 5 (2016).","chicago":"Vyleta, Nicholas, Carolina Borges Merjane, and Peter M Jonas. “Plasticity-Dependent, Full Detonation at Hippocampal Mossy Fiber–CA3 Pyramidal Neuron Synapses.” <i>ELife</i>. eLife Sciences Publications, 2016. <a href=\"https://doi.org/10.7554/eLife.17977\">https://doi.org/10.7554/eLife.17977</a>.","ieee":"N. Vyleta, C. Borges Merjane, and P. M. Jonas, “Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses,” <i>eLife</i>, vol. 5. eLife Sciences Publications, 2016.","apa":"Vyleta, N., Borges Merjane, C., &#38; Jonas, P. M. (2016). Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.17977\">https://doi.org/10.7554/eLife.17977</a>","ama":"Vyleta N, Borges Merjane C, Jonas PM. Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. <i>eLife</i>. 2016;5. doi:<a href=\"https://doi.org/10.7554/eLife.17977\">10.7554/eLife.17977</a>","mla":"Vyleta, Nicholas, et al. “Plasticity-Dependent, Full Detonation at Hippocampal Mossy Fiber–CA3 Pyramidal Neuron Synapses.” <i>ELife</i>, vol. 5, e17977, eLife Sciences Publications, 2016, doi:<a href=\"https://doi.org/10.7554/eLife.17977\">10.7554/eLife.17977</a>.","ista":"Vyleta N, Borges Merjane C, Jonas PM. 2016. Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses. eLife. 5, e17977."},"article_number":"e17977","day":"25","quality_controlled":"1","publisher":"eLife Sciences Publications","file_date_updated":"2020-07-14T12:44:44Z","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"PeJo"}],"has_accepted_license":"1","status":"public","title":"Plasticity-dependent, full detonation at hippocampal mossy fiber–CA3 pyramidal neuron synapses","publication":"eLife","project":[{"call_identifier":"FP7","grant_number":"268548","_id":"25C0F108-B435-11E9-9278-68D0E5697425","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"},{"name":"Biophysics and circuit function of a giant cortical glumatergic synapse","_id":"25B7EB9E-B435-11E9-9278-68D0E5697425","call_identifier":"H2020","grant_number":"692692"}],"publist_id":"5947","_id":"1323","date_created":"2018-12-11T11:51:22Z","date_published":"2016-10-25T00:00:00Z","scopus_import":1,"pubrep_id":"715","author":[{"id":"36C4978E-F248-11E8-B48F-1D18A9856A87","full_name":"Vyleta, Nicholas","last_name":"Vyleta","first_name":"Nicholas"},{"last_name":"Borges Merjane","orcid":"0000-0003-0005-401X","first_name":"Carolina","full_name":"Borges Merjane, Carolina","id":"4305C450-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"ec_funded":1,"abstract":[{"lang":"eng","text":"Mossy fiber synapses on CA3 pyramidal cells are 'conditional detonators' that reliably discharge postsynaptic targets. The 'conditional' nature implies that burst activity in dentate gyrus granule cells is required for detonation. Whether single unitary excitatory postsynaptic potentials (EPSPs) trigger spikes in CA3 neurons remains unknown. Mossy fiber synapses exhibit both pronounced short-term facilitation and uniquely large post-tetanic potentiation (PTP). We tested whether PTP could convert mossy fiber synapses from subdetonator into detonator mode, using a recently developed method to selectively and noninvasively stimulate individual presynaptic terminals in rat brain slices. Unitary EPSPs failed to initiate a spike in CA3 neurons under control conditions, but reliably discharged them after induction of presynaptic short-term plasticity. Remarkably, PTP switched mossy fiber synapses into full detonators for tens of seconds. Plasticity-dependent detonation may be critical for efficient coding, storage, and recall of information in the granule cell–CA3 cell network."}],"type":"journal_article","date_updated":"2023-02-21T10:34:24Z","acknowledged_ssus":[{"_id":"M-Shop"},{"_id":"PreCl"}],"publication_status":"published","intvolume":"         5","language":[{"iso":"eng"}],"month":"10","ddc":["571","572"],"doi":"10.7554/eLife.17977","year":"2016"},{"publist_id":"5899","project":[{"name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","grant_number":"268548","call_identifier":"FP7","_id":"25C0F108-B435-11E9-9278-68D0E5697425"},{"name":"Mechanisms of transmitter release at GABAergic synapses","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","call_identifier":"FWF","grant_number":"P24909-B24"}],"publication":"Science","has_accepted_license":"1","status":"public","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"title":"Synaptic mechanisms of pattern completion in the hippocampal CA3 network","file_date_updated":"2020-07-14T12:44:46Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publisher":"American Association for the Advancement of Science","quality_controlled":"1","day":"09","oa":1,"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.","apa":"Guzmán, J., Schlögl, A., Frotscher, M., &#38; Jonas, P. M. (2016). Synaptic mechanisms of pattern completion in the hippocampal CA3 network. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.aaf1836\">https://doi.org/10.1126/science.aaf1836</a>","mla":"Guzmán, José, et al. “Synaptic Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” <i>Science</i>, vol. 353, no. 6304, American Association for the Advancement of Science, 2016, pp. 1117–23, doi:<a href=\"https://doi.org/10.1126/science.aaf1836\">10.1126/science.aaf1836</a>.","ama":"Guzmán J, Schlögl A, Frotscher M, Jonas PM. Synaptic mechanisms of pattern completion in the hippocampal CA3 network. <i>Science</i>. 2016;353(6304):1117-1123. doi:<a href=\"https://doi.org/10.1126/science.aaf1836\">10.1126/science.aaf1836</a>","ieee":"J. Guzmán, A. Schlögl, M. Frotscher, and P. M. Jonas, “Synaptic mechanisms of pattern completion in the hippocampal CA3 network,” <i>Science</i>, vol. 353, no. 6304. American Association for the Advancement of Science, pp. 1117–1123, 2016.","chicago":"Guzmán, José, Alois Schlögl, Michael Frotscher, and Peter M Jonas. “Synaptic Mechanisms of Pattern Completion in the Hippocampal CA3 Network.” <i>Science</i>. American Association for the Advancement of Science, 2016. <a href=\"https://doi.org/10.1126/science.aaf1836\">https://doi.org/10.1126/science.aaf1836</a>.","short":"J. Guzmán, A. Schlögl, M. Frotscher, P.M. Jonas, Science 353 (2016) 1117–1123."},"file":[{"date_created":"2018-12-12T10:12:27Z","date_updated":"2020-07-14T12:44:46Z","checksum":"89caefa4e181424cbf0aecc835fcc5ec","access_level":"open_access","file_size":19408143,"file_name":"IST-2017-823-v1+1_aaf1836_CombinedPDF_v2-1.pdf","relation":"main_file","content_type":"application/pdf","file_id":"4945","creator":"system"}],"volume":353,"oa_version":"Preprint","page":"1117 - 1123","doi":"10.1126/science.aaf1836","year":"2016","ddc":["570"],"month":"09","language":[{"iso":"eng"}],"publication_status":"published","intvolume":"       353","acknowledged_ssus":[{"_id":"ScienComp"}],"type":"journal_article","date_updated":"2021-01-12T06:50:04Z","ec_funded":1,"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."}],"author":[{"id":"30CC5506-F248-11E8-B48F-1D18A9856A87","full_name":"Guzmán, José","last_name":"Guzmán","first_name":"José"},{"first_name":"Alois","orcid":"0000-0002-5621-8100","last_name":"Schlögl","full_name":"Schlögl, Alois","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87"},{"last_name":"Frotscher","first_name":"Michael","full_name":"Frotscher, Michael"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","first_name":"Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","full_name":"Jonas, Peter M"}],"issue":"6304","pubrep_id":"823","date_published":"2016-09-09T00:00:00Z","scopus_import":1,"date_created":"2018-12-11T11:51:31Z","_id":"1350"},{"date_published":"2016-03-01T00:00:00Z","_id":"1396","degree_awarded":"PhD","date_created":"2018-12-11T11:51:46Z","supervisor":[{"full_name":"Jonas, Peter M","first_name":"Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"author":[{"first_name":"Rajiv Kumar","last_name":"Mishra","full_name":"Mishra, Rajiv Kumar","id":"46CB58F2-F248-11E8-B48F-1D18A9856A87"}],"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."}],"related_material":{"record":[{"id":"1432","relation":"part_of_dissertation","status":"public"}]},"publication_status":"published","date_updated":"2023-09-07T11:55:26Z","type":"dissertation","ddc":["570"],"year":"2016","language":[{"iso":"eng"}],"month":"03","alternative_title":["ISTA Thesis"],"oa_version":"Published Version","page":"83","file":[{"file_size":2407572,"content_type":"application/pdf","relation":"main_file","file_name":"Thesis_Mishra_Rajiv (Final).pdf","file_id":"6782","creator":"dernst","date_created":"2019-08-09T12:14:46Z","date_updated":"2020-07-14T12:44:48Z","checksum":"5a010a838faf040f7064f3cfb802f743","access_level":"closed"},{"file_size":2407572,"file_name":"2016_RajivMishra_Thesis.pdf","relation":"main_file","content_type":"application/pdf","file_id":"9183","creator":"dernst","success":1,"date_created":"2021-02-22T11:48:44Z","date_updated":"2021-02-22T11:48:44Z","checksum":"81b26d9ede92c99f1d8cc6fa1d04cbbb","access_level":"open_access"}],"publication_identifier":{"issn":["2663-337X"]},"citation":{"ieee":"R. K. Mishra, “Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus,” Institute of Science and Technology Austria, 2016.","chicago":"Mishra, Rajiv Kumar. “Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus.” Institute of Science and Technology Austria, 2016.","short":"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. <i>Synaptic Plasticity Rules at CA3-CA3 Recurrent Synapses in Hippocampus</i>. 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). <i>Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus</i>. Institute of Science and Technology Austria."},"oa":1,"day":"01","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","file_date_updated":"2021-02-22T11:48:44Z","has_accepted_license":"1","department":[{"_id":"PeJo"}],"title":"Synaptic plasticity rules at CA3-CA3 recurrent synapses in hippocampus","status":"public","publisher":"Institute of Science and Technology Austria","publist_id":"5811","article_processing_charge":"No"},{"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file_date_updated":"2023-05-16T07:03:56Z","title":"High performance computing at IST Austria: Modelling the human hippocampus","has_accepted_license":"1","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"status":"public","publication_status":"published","date_updated":"2023-05-16T07:15:14Z","type":"conference_abstract","publisher":"VSC - Vienna Scientific Cluster","ddc":["000"],"year":"2016","article_processing_charge":"No","language":[{"iso":"eng"}],"month":"02","publication":"AHPC16 - Austrian HPC Meeting 2016","main_file_link":[{"url":"https://vsc.ac.at/fileadmin/user_upload/vsc/conferences/ahpc16/BOOKLET_AHPC16.pdf","open_access":"1"}],"date_published":"2016-02-24T00:00:00Z","conference":{"end_date":"2016-02-24","name":"AHPC: Austrian HPC Meeting","start_date":"2016-02-22","location":"Grundlsee, Austria"},"_id":"12903","page":"37","oa_version":"Published Version","file":[{"date_updated":"2023-05-16T07:03:56Z","date_created":"2023-05-16T07:03:56Z","access_level":"open_access","checksum":"4a7b00362e81358d568f5e216fa03c3e","file_size":1073523,"success":1,"creator":"dernst","file_id":"12968","relation":"main_file","content_type":"application/pdf","file_name":"2016_AHPC_Schloegl.pdf"}],"date_created":"2023-05-05T12:54:47Z","author":[{"full_name":"Schlögl, Alois","first_name":"Alois","orcid":"0000-0002-5621-8100","last_name":"Schlögl","id":"45BF87EE-F248-11E8-B48F-1D18A9856A87"},{"id":"4D0BC184-F248-11E8-B48F-1D18A9856A87","first_name":"Stephan","last_name":"Stadlbauer","full_name":"Stadlbauer, Stephan"}],"quality_controlled":"1","citation":{"short":"A. Schlögl, S. Stadlbauer, in:, 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 <i>AHPC16 - Austrian HPC Meeting 2016</i>, Grundlsee, Austria, 2016, p. 37.","chicago":"Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST Austria: Modelling the Human Hippocampus.” In <i>AHPC16 - Austrian HPC Meeting 2016</i>, 37. VSC - Vienna Scientific Cluster, 2016.","mla":"Schlögl, Alois, and Stephan Stadlbauer. “High Performance Computing at IST Austria: Modelling the Human Hippocampus.” <i>AHPC16 - Austrian HPC Meeting 2016</i>, VSC - Vienna Scientific Cluster, 2016, p. 37.","ama":"Schlögl A, Stadlbauer S. High performance computing at IST Austria: Modelling the human hippocampus. In: <i>AHPC16 - Austrian HPC Meeting 2016</i>. VSC - Vienna Scientific Cluster; 2016:37.","apa":"Schlögl, A., &#38; Stadlbauer, S. (2016). High performance computing at IST Austria: Modelling the human hippocampus. In <i>AHPC16 - Austrian HPC Meeting 2016</i> (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."},"oa":1,"day":"24"},{"type":"journal_article","date_updated":"2021-01-12T06:52:01Z","publication_status":"published","intvolume":"        13","month":"10","language":[{"iso":"eng"}],"doi":"10.1016/j.celrep.2015.09.011","year":"2015","ddc":["570"],"date_created":"2018-12-11T11:53:02Z","_id":"1615","date_published":"2015-10-20T00:00:00Z","scopus_import":1,"pubrep_id":"470","author":[{"full_name":"Hammer, Matthieu","last_name":"Hammer","first_name":"Matthieu"},{"full_name":"Krueger Burg, Dilja","first_name":"Dilja","last_name":"Krueger Burg"},{"first_name":"Liam","last_name":"Tuffy","full_name":"Tuffy, Liam"},{"full_name":"Cooper, Benjamin","last_name":"Cooper","first_name":"Benjamin"},{"full_name":"Taschenberger, Holger","last_name":"Taschenberger","first_name":"Holger"},{"id":"3A578F32-F248-11E8-B48F-1D18A9856A87","full_name":"Goswami, Sarit","last_name":"Goswami","first_name":"Sarit"},{"last_name":"Ehrenreich","first_name":"Hannelore","full_name":"Ehrenreich, Hannelore"},{"full_name":"Jonas, Peter M","first_name":"Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Frederique","last_name":"Varoqueaux","full_name":"Varoqueaux, Frederique"},{"last_name":"Rhee","first_name":"Jeong","full_name":"Rhee, Jeong"},{"full_name":"Brose, Nils","last_name":"Brose","first_name":"Nils"}],"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","publisher":"Cell Press","department":[{"_id":"PeJo"}],"title":"Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism","has_accepted_license":"1","status":"public","file_date_updated":"2020-07-14T12:45:07Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","publication":"Cell Reports","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.","publist_id":"5551","file":[{"date_created":"2018-12-12T10:13:23Z","date_updated":"2020-07-14T12:45:07Z","access_level":"open_access","checksum":"44d30fbb543774b076b4938bd36af9d7","file_size":2314406,"file_name":"IST-2016-470-v1+1_1-s2.0-S2211124715010220-main.pdf","relation":"main_file","content_type":"application/pdf","file_id":"5005","creator":"system"}],"oa_version":"Published Version","volume":13,"page":"516 - 523","tmp":{"image":"/images/cc_by.png","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)"},"day":"20","oa":1,"citation":{"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.","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.” <i>Cell Reports</i>. Cell Press, 2015. <a href=\"https://doi.org/10.1016/j.celrep.2015.09.011\">https://doi.org/10.1016/j.celrep.2015.09.011</a>.","ieee":"M. Hammer <i>et al.</i>, “Perturbed hippocampal synaptic inhibition and γ-oscillations in a neuroligin-4 knockout mouse model of autism,” <i>Cell Reports</i>, vol. 13, no. 3. Cell Press, pp. 516–523, 2015.","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. <i>Cell Reports</i>. Cell Press. <a href=\"https://doi.org/10.1016/j.celrep.2015.09.011\">https://doi.org/10.1016/j.celrep.2015.09.011</a>","mla":"Hammer, Matthieu, et al. “Perturbed Hippocampal Synaptic Inhibition and γ-Oscillations in a Neuroligin-4 Knockout Mouse Model of Autism.” <i>Cell Reports</i>, vol. 13, no. 3, Cell Press, 2015, pp. 516–23, doi:<a href=\"https://doi.org/10.1016/j.celrep.2015.09.011\">10.1016/j.celrep.2015.09.011</a>.","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. <i>Cell Reports</i>. 2015;13(3):516-523. doi:<a href=\"https://doi.org/10.1016/j.celrep.2015.09.011\">10.1016/j.celrep.2015.09.011</a>","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."},"quality_controlled":"1"},{"citation":{"ista":"Chen C, Wang C, Zhao X, Zhou T, Xu D, Wang Z, Wang Y. 2015. Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. ASN Neuro. 7(2).","apa":"Chen, C., Wang, C., Zhao, X., Zhou, T., Xu, D., Wang, Z., &#38; Wang, Y. (2015). Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. <i>ASN Neuro</i>. SAGE Publications. <a href=\"https://doi.org/10.1177/1759091415575845\">https://doi.org/10.1177/1759091415575845</a>","ama":"Chen C, Wang C, Zhao X, et al. Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats. <i>ASN Neuro</i>. 2015;7(2). doi:<a href=\"https://doi.org/10.1177/1759091415575845\">10.1177/1759091415575845</a>","mla":"Chen, Chong, et al. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” <i>ASN Neuro</i>, vol. 7, no. 2, SAGE Publications, 2015, doi:<a href=\"https://doi.org/10.1177/1759091415575845\">10.1177/1759091415575845</a>.","chicago":"Chen, Chong, Chao Wang, Xuan Zhao, Tao Zhou, Dao Xu, Zhi Wang, and Ying Wang. “Low-Dose Sevoflurane Promoteshippocampal Neurogenesis and Facilitates the Development of Dentate Gyrus-Dependent Learning in Neonatal Rats.” <i>ASN Neuro</i>. SAGE Publications, 2015. <a href=\"https://doi.org/10.1177/1759091415575845\">https://doi.org/10.1177/1759091415575845</a>.","ieee":"C. Chen <i>et al.</i>, “Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats,” <i>ASN Neuro</i>, vol. 7, no. 2. SAGE Publications, 2015.","short":"C. Chen, C. Wang, X. Zhao, T. Zhou, D. Xu, Z. Wang, Y. Wang, ASN Neuro 7 (2015)."},"oa":1,"day":"13","quality_controlled":"1","article_type":"original","volume":7,"oa_version":"Published Version","file":[{"date_created":"2018-12-12T10:14:08Z","date_updated":"2020-07-14T12:45:18Z","checksum":"53e16bd3fc2ae2c0d7de9164626c37aa","access_level":"open_access","file_size":1146814,"relation":"main_file","content_type":"application/pdf","file_name":"IST-2016-456-v1+1_ASN_Neuro-2015-Chen-.pdf","file_id":"5057","creator":"system"}],"tmp":{"name":"Creative Commons Attribution 3.0 Unported (CC BY 3.0)","image":"/images/cc_by.png","short":"CC BY (3.0)","legal_code_url":"https://creativecommons.org/licenses/by/3.0/legalcode"},"article_processing_charge":"No","publication":"ASN Neuro","publist_id":"5269","publisher":"SAGE Publications","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file_date_updated":"2020-07-14T12:45:18Z","department":[{"_id":"PeJo"}],"title":"Low-dose sevoflurane promoteshippocampal neurogenesis and facilitates the development of dentate gyrus-dependent learning in neonatal rats","status":"public","has_accepted_license":"1","pubrep_id":"456","issue":"2","abstract":[{"lang":"eng","text":"Huge body of evidences demonstrated that volatile anesthetics affect the hippocampal neurogenesis and neurocognitive functions, and most of them showed impairment at anesthetic dose. Here, we investigated the effect of low dose (1.8%) sevoflurane on hippocampal neurogenesis and dentate gyrus-dependent learning. Neonatal rats at postnatal day 4 to 6 (P4-6) were treated with 1.8% sevoflurane for 6 hours. Neurogenesis was quantified by bromodeoxyuridine labeling and electrophysiology recording. Four and seven weeks after treatment, the Morris water maze and contextual-fear discrimination learning tests were performed to determine the influence on spatial learning and pattern separation. A 6-hour treatment with 1.8% sevoflurane promoted hippocampal neurogenesis and increased the survival of newborn cells and the proportion of immature granular cells in the dentate gyrus of neonatal rats. Sevoflurane-treated rats performed better during the training days of the Morris water maze test and in contextual-fear discrimination learning test. These results suggest that a subanesthetic dose of sevoflurane promotes hippocampal neurogenesis in neonatal rats and facilitates their performance in dentate gyrus-dependent learning tasks."}],"author":[{"id":"3DFD581A-F248-11E8-B48F-1D18A9856A87","first_name":"Chong","last_name":"Chen","full_name":"Chen, Chong"},{"first_name":"Chao","last_name":"Wang","full_name":"Wang, Chao"},{"full_name":"Zhao, Xuan","last_name":"Zhao","first_name":"Xuan"},{"full_name":"Zhou, Tao","first_name":"Tao","last_name":"Zhou"},{"last_name":"Xu","first_name":"Dao","full_name":"Xu, Dao"},{"full_name":"Wang, Zhi","last_name":"Wang","first_name":"Zhi"},{"full_name":"Wang, Ying","first_name":"Ying","last_name":"Wang"}],"_id":"1834","date_created":"2018-12-11T11:54:16Z","license":"https://creativecommons.org/licenses/by/3.0/","scopus_import":"1","date_published":"2015-04-13T00:00:00Z","language":[{"iso":"eng"}],"month":"04","ddc":["570"],"year":"2015","doi":"10.1177/1759091415575845","date_updated":"2023-10-18T06:47:30Z","type":"journal_article","intvolume":"         7","publication_status":"published"},{"month":"03","language":[{"iso":"eng"}],"year":"2015","doi":"10.1016/j.neuron.2015.03.006","ddc":["570"],"date_updated":"2021-10-08T09:07:34Z","type":"journal_article","intvolume":"        85","publication_status":"published","pubrep_id":"822","abstract":[{"lang":"eng","text":"Based on extrapolation from excitatory synapses, it is often assumed that depletion of the releasable pool of synaptic vesicles is the main factor underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba (2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes in presynaptic action potential waveform substantially contribute to synaptic depression. Based on extrapolation from excitatory synapses, it is often assumed that depletion of the releasable pool of synaptic vesicles is the main factor underlying depression at inhibitory synapses. In this issue of Neuron, using subcellular patch-clamp recording from inhibitory presynaptic terminals, Kawaguchi and Sakaba (2015) show that at Purkinje cell-deep cerebellar nuclei neuron synapses, changes in presynaptic action potential waveform substantially contribute to synaptic depression."}],"author":[{"full_name":"Vandael, David H","last_name":"Vandael","orcid":"0000-0001-7577-1676","first_name":"David H","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87"},{"first_name":"Claudia ","orcid":"0000-0003-4710-2082","last_name":"Espinoza Martinez","full_name":"Espinoza Martinez, Claudia ","id":"31FFEE2E-F248-11E8-B48F-1D18A9856A87"},{"id":"353C1B58-F248-11E8-B48F-1D18A9856A87","last_name":"Jonas","orcid":"0000-0001-5001-4804","first_name":"Peter M","full_name":"Jonas, Peter M"}],"issue":"6","date_created":"2018-12-11T11:54:19Z","_id":"1845","scopus_import":"1","date_published":"2015-03-18T00:00:00Z","license":"https://creativecommons.org/licenses/by-nc/4.0/","publication":"Neuron","article_processing_charge":"No","publist_id":"5256","publisher":"Elsevier","department":[{"_id":"PeJo"}],"title":"Excitement about inhibitory presynaptic terminals","status":"public","has_accepted_license":"1","user_id":"8b945eb4-e2f2-11eb-945a-df72226e66a9","file_date_updated":"2020-07-14T12:45:19Z","day":"18","citation":{"short":"D.H. Vandael, C. Espinoza Martinez, P.M. Jonas, Neuron 85 (2015) 1149–1151.","ieee":"D. H. Vandael, C. Espinoza Martinez, and P. M. Jonas, “Excitement about inhibitory presynaptic terminals,” <i>Neuron</i>, vol. 85, no. 6. Elsevier, pp. 1149–1151, 2015.","chicago":"Vandael, David H, Claudia  Espinoza Martinez, and Peter M Jonas. “Excitement about Inhibitory Presynaptic Terminals.” <i>Neuron</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.neuron.2015.03.006\">https://doi.org/10.1016/j.neuron.2015.03.006</a>.","ama":"Vandael DH, Espinoza Martinez C, Jonas PM. Excitement about inhibitory presynaptic terminals. <i>Neuron</i>. 2015;85(6):1149-1151. doi:<a href=\"https://doi.org/10.1016/j.neuron.2015.03.006\">10.1016/j.neuron.2015.03.006</a>","mla":"Vandael, David H., et al. “Excitement about Inhibitory Presynaptic Terminals.” <i>Neuron</i>, vol. 85, no. 6, Elsevier, 2015, pp. 1149–51, doi:<a href=\"https://doi.org/10.1016/j.neuron.2015.03.006\">10.1016/j.neuron.2015.03.006</a>.","apa":"Vandael, D. H., Espinoza Martinez, C., &#38; Jonas, P. M. (2015). Excitement about inhibitory presynaptic terminals. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2015.03.006\">https://doi.org/10.1016/j.neuron.2015.03.006</a>","ista":"Vandael DH, Espinoza Martinez C, Jonas PM. 2015. Excitement about inhibitory presynaptic terminals. Neuron. 85(6), 1149–1151."},"oa":1,"quality_controlled":"1","file":[{"date_created":"2018-12-12T10:16:07Z","date_updated":"2020-07-14T12:45:19Z","access_level":"open_access","checksum":"d1808550e376a0eca2a950fda017cfa6","file_size":411832,"file_name":"IST-2017-822-v1+1_Perspective_Fig__Final.pdf","content_type":"application/pdf","relation":"main_file","creator":"system","file_id":"5192"},{"access_level":"open_access","checksum":"a279f4ae61e6c8f33d68f69a0d02097d","date_updated":"2020-07-14T12:45:19Z","date_created":"2018-12-12T10:16:07Z","creator":"system","file_id":"5193","file_name":"IST-2017-822-v1+2_Perspective_Final2.pdf","content_type":"application/pdf","relation":"main_file","file_size":100769}],"volume":85,"oa_version":"Published Version","page":"1149 - 1151","tmp":{"short":"CC BY-NC (4.0)","legal_code_url":"https://creativecommons.org/licenses/by-nc/4.0/legalcode","name":"Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0)","image":"/images/cc_by_nc.png"}},{"month":"10","language":[{"iso":"eng"}],"doi":"10.2174/1874467208666150507105443","year":"2015","type":"journal_article","date_updated":"2021-01-12T06:51:26Z","publication_status":"published","intvolume":"         8","abstract":[{"text":"Neuronal and neuroendocrine L-type calcium channels (Cav1.2, Cav1.3) open readily at relatively low membrane potentials and allow Ca2+ to enter the cells near resting potentials. In this way, Cav1.2 and Cav1.3 shape the action potential waveform, contribute to gene expression, synaptic plasticity, neuronal differentiation, hormone secretion and pacemaker activity. In the chromaffin cells (CCs) of the adrenal medulla, Cav1.3 is highly expressed and is shown to support most of the pacemaking current that sustains action potential (AP) firings and part of the catecholamine secretion. Cav1.3 forms Ca2+-nanodomains with the fast inactivating BK channels and drives the resting SK currents. These latter set the inter-spike interval duration between consecutive spikes during spontaneous firing and the rate of spike adaptation during sustained depolarizations. Cav1.3 plays also a primary role in the switch from “tonic” to “burst” firing that occurs in mouse CCs when either the availability of voltage-gated Na channels (Nav) is reduced or the β2 subunit featuring the fast inactivating BK channels is deleted. Here, we discuss the functional role of these “neuronlike” firing modes in CCs and how Cav1.3 contributes to them. The open issue is to understand how these novel firing patterns are adapted to regulate the quantity of circulating catecholamines during resting condition or in response to acute and chronic stress.","lang":"eng"}],"author":[{"full_name":"Vandael, David H","orcid":"0000-0001-7577-1676","last_name":"Vandael","first_name":"David H","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Marcantoni, Andrea","last_name":"Marcantoni","first_name":"Andrea"},{"last_name":"Carbone","first_name":"Emilio","full_name":"Carbone, Emilio"}],"issue":"2","date_created":"2018-12-11T11:52:35Z","_id":"1535","date_published":"2015-10-01T00:00:00Z","scopus_import":1,"pmid":1,"publication":"Current Molecular Pharmacology","article_processing_charge":"No","acknowledgement":"This work was supported by the Italian MIUR (PRIN 2010/2011 project 2010JFYFY2) and the University of Torino.","external_id":{"pmid":["25966692"]},"publist_id":"5636","publisher":"Bentham Science Publishers","title":"Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells","status":"public","department":[{"_id":"PeJo"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","day":"01","oa":1,"citation":{"apa":"Vandael, D. H., Marcantoni, A., &#38; Carbone, E. (2015). Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. <i>Current Molecular Pharmacology</i>. Bentham Science Publishers. <a href=\"https://doi.org/10.2174/1874467208666150507105443\">https://doi.org/10.2174/1874467208666150507105443</a>","mla":"Vandael, David H., et al. “Cav1.3 Channels as Key Regulators of Neuron-like Firings and Catecholamine Release in Chromaffin Cells.” <i>Current Molecular Pharmacology</i>, vol. 8, no. 2, Bentham Science Publishers, 2015, pp. 149–61, doi:<a href=\"https://doi.org/10.2174/1874467208666150507105443\">10.2174/1874467208666150507105443</a>.","ama":"Vandael DH, Marcantoni A, Carbone E. Cav1.3 channels as key regulators of neuron-like firings and catecholamine release in chromaffin cells. <i>Current Molecular Pharmacology</i>. 2015;8(2):149-161. doi:<a href=\"https://doi.org/10.2174/1874467208666150507105443\">10.2174/1874467208666150507105443</a>","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.","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.” <i>Current Molecular Pharmacology</i>. Bentham Science Publishers, 2015. <a href=\"https://doi.org/10.2174/1874467208666150507105443\">https://doi.org/10.2174/1874467208666150507105443</a>.","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,” <i>Current Molecular Pharmacology</i>, vol. 8, no. 2. Bentham Science Publishers, pp. 149–161, 2015."},"quality_controlled":"1","oa_version":"Submitted Version","page":"149 - 161","volume":8,"article_type":"original","main_file_link":[{"url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5384372/","open_access":"1"}]},{"intvolume":"       593","publication_status":"published","date_updated":"2021-01-12T06:51:38Z","type":"journal_article","year":"2015","doi":"10.1113/JP271078","language":[{"iso":"eng"}],"month":"11","pmid":1,"scopus_import":1,"date_published":"2015-11-15T00:00:00Z","_id":"1565","date_created":"2018-12-11T11:52:45Z","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"}],"author":[{"full_name":"Gavello, Daniela","last_name":"Gavello","first_name":"Daniela"},{"full_name":"Vandael, David H","orcid":"0000-0001-7577-1676","last_name":"Vandael","first_name":"David H","id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Gosso, Sara","first_name":"Sara","last_name":"Gosso"},{"last_name":"Carbone","first_name":"Emilio","full_name":"Carbone, Emilio"},{"last_name":"Carabelli","first_name":"Valentina","full_name":"Carabelli, Valentina"}],"user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"PeJo"}],"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","status":"public","publisher":"Wiley-Blackwell","publist_id":"5606","acknowledgement":"This work was supported by the Compagnia di San Paolo Foundation ‘Neuroscience Program’ to VC and ‘Progetto di Ateneo 2011-13’ to EC.\r\nWe thank Dr Claudio Franchino for cell preparation and for providing excellent technical support.","external_id":{"pmid":["26282459"]},"publication":"Journal of Physiology","main_file_link":[{"open_access":"1","url":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4650409/"}],"oa_version":"Submitted Version","page":"4835 - 4853","volume":593,"quality_controlled":"1","citation":{"short":"D. Gavello, D.H. Vandael, S. Gosso, E. Carbone, V. Carabelli, Journal of Physiology 593 (2015) 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,” <i>Journal of Physiology</i>, vol. 593, no. 22. Wiley-Blackwell, pp. 4835–4853, 2015.","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.” <i>Journal of Physiology</i>. Wiley-Blackwell, 2015. <a href=\"https://doi.org/10.1113/JP271078\">https://doi.org/10.1113/JP271078</a>.","apa":"Gavello, D., Vandael, D. H., Gosso, S., Carbone, E., &#38; 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. <i>Journal of Physiology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1113/JP271078\">https://doi.org/10.1113/JP271078</a>","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.” <i>Journal of Physiology</i>, vol. 593, no. 22, Wiley-Blackwell, 2015, pp. 4835–53, doi:<a href=\"https://doi.org/10.1113/JP271078\">10.1113/JP271078</a>.","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. <i>Journal of Physiology</i>. 2015;593(22):4835-4853. doi:<a href=\"https://doi.org/10.1113/JP271078\">10.1113/JP271078</a>","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."},"oa":1,"day":"15"},{"file_date_updated":"2020-07-14T12:45:02Z","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"PeJo"}],"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","has_accepted_license":"1","publisher":"Elsevier","publist_id":"5591","article_processing_charge":"No","publication":"Neuroscience","tmp":{"short":"CC BY-NC-ND (4.0)","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)","image":"/images/cc_by_nc_nd.png"},"volume":311,"oa_version":"Submitted Version","page":"430 - 443","article_type":"original","file":[{"checksum":"af2c4c994718c7be417eba0dc746aac9","access_level":"open_access","date_updated":"2020-07-14T12:45:02Z","date_created":"2020-05-15T06:50:20Z","file_id":"7849","creator":"dernst","content_type":"application/pdf","relation":"main_file","file_name":"2015_Neuroscience_Brenes.pdf","file_size":5563015}],"quality_controlled":"1","oa":1,"citation":{"apa":"Brenes, O., Vandael, D. H., Carbone, E., Montarolo, P., &#38; 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. <i>Neuroscience</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuroscience.2015.10.046\">https://doi.org/10.1016/j.neuroscience.2015.10.046</a>","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. <i>Neuroscience</i>. 2015;311:430-443. doi:<a href=\"https://doi.org/10.1016/j.neuroscience.2015.10.046\">10.1016/j.neuroscience.2015.10.046</a>","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.” <i>Neuroscience</i>, vol. 311, Elsevier, 2015, pp. 430–43, doi:<a href=\"https://doi.org/10.1016/j.neuroscience.2015.10.046\">10.1016/j.neuroscience.2015.10.046</a>.","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.","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.” <i>Neuroscience</i>. Elsevier, 2015. <a href=\"https://doi.org/10.1016/j.neuroscience.2015.10.046\">https://doi.org/10.1016/j.neuroscience.2015.10.046</a>.","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,” <i>Neuroscience</i>, vol. 311. Elsevier, pp. 430–443, 2015."},"day":"17","publication_status":"published","intvolume":"       311","type":"journal_article","date_updated":"2021-01-12T06:51:44Z","ddc":["570"],"doi":"10.1016/j.neuroscience.2015.10.046","year":"2015","language":[{"iso":"eng"}],"month":"12","date_published":"2015-12-17T00:00:00Z","scopus_import":1,"_id":"1580","date_created":"2018-12-11T11:52:50Z","abstract":[{"text":"Synapsins (Syns) are an evolutionarily conserved family of presynaptic proteins crucial for the fine-tuning of synaptic function. A large amount of experimental evidences has shown that Syns are involved in the development of epileptic phenotypes and several mutations in Syn genes have been associated with epilepsy in humans and animal models. Syn mutations induce alterations in circuitry and neurotransmitter release, differentially affecting excitatory and inhibitory synapses, thus causing an excitation/inhibition imbalance in network excitability toward hyperexcitability that may be a determinant with regard to the development of epilepsy. Another approach to investigate epileptogenic mechanisms is to understand how silencing Syn affects the cellular behavior of single neurons and is associated with the hyperexcitable phenotypes observed in epilepsy. Here, we examined the functional effects of antisense-RNA inhibition of Syn expression on individually identified and isolated serotonergic cells of the Helix land snail. We found that Helix synapsin silencing increases cell excitability characterized by a slightly depolarized resting membrane potential, decreases the rheobase, reduces the threshold for action potential (AP) firing and increases the mean and instantaneous firing rates, with respect to control cells. The observed increase of Ca2+ and BK currents in Syn-silenced cells seems to be related to changes in the shape of the AP waveform. These currents sustain the faster spiking in Syn-deficient cells by increasing the after hyperpolarization and limiting the Na+ and Ca2+ channel inactivation during repetitive firing. This in turn speeds up the depolarization phase by reaching the AP threshold faster. Our results provide evidence that Syn silencing increases intrinsic cell excitability associated with increased Ca2+ and Ca2+-dependent BK currents in the absence of excitatory or inhibitory inputs.","lang":"eng"}],"author":[{"last_name":"Brenes","first_name":"Oscar","full_name":"Brenes, Oscar"},{"id":"3AE48E0A-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-7577-1676","last_name":"Vandael","first_name":"David H","full_name":"Vandael, David H"},{"first_name":"Emilio","last_name":"Carbone","full_name":"Carbone, Emilio"},{"full_name":"Montarolo, Pier","last_name":"Montarolo","first_name":"Pier"},{"full_name":"Ghirardi, Mirella","last_name":"Ghirardi","first_name":"Mirella"}]},{"ddc":["570"],"year":"2015","doi":"10.1073/pnas.1412996112","language":[{"iso":"eng"}],"month":"01","intvolume":"       112","publication_status":"published","date_updated":"2021-01-12T06:52:01Z","type":"journal_article","issue":"4","abstract":[{"lang":"eng","text":"GABAergic perisoma-inhibiting fast-spiking interneurons (PIIs) effectively control the activity of large neuron populations by their wide axonal arborizations. It is generally assumed that the output of one PII to its target cells is strong and rapid. Here, we show that, unexpectedly, both strength and time course of PII-mediated perisomatic inhibition change with distance between synaptically connected partners in the rodent hippocampus. Synaptic signals become weaker due to lower contact numbers and decay more slowly with distance, very likely resulting from changes in GABAA receptor subunit composition. When distance-dependent synaptic inhibition is introduced to a rhythmically active neuronal network model, randomly driven principal cell assemblies are strongly synchronized by the PIIs, leading to higher precision in principal cell spike times than in a network with uniform synaptic inhibition. "}],"author":[{"last_name":"Strüber","first_name":"Michael","full_name":"Strüber, Michael"},{"last_name":"Jonas","orcid":"0000-0001-5001-4804","first_name":"Peter M","full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Bartos, Marlene","last_name":"Bartos","first_name":"Marlene"}],"ec_funded":1,"pmid":1,"scopus_import":1,"date_published":"2015-01-27T00:00:00Z","_id":"1614","date_created":"2018-12-11T11:53:02Z","project":[{"name":"Mechanisms of transmitter release at GABAergic synapses","_id":"25C26B1E-B435-11E9-9278-68D0E5697425","grant_number":"P24909-B24","call_identifier":"FWF"},{"name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","_id":"25C0F108-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"268548"}],"publist_id":"5552","external_id":{"pmid":["25583495"]},"publication":"PNAS","user_id":"2DF688A6-F248-11E8-B48F-1D18A9856A87","file_date_updated":"2020-07-14T12:45:07Z","title":"Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells","status":"public","department":[{"_id":"PeJo"}],"has_accepted_license":"1","publisher":"National Academy of Sciences","quality_controlled":"1","citation":{"ieee":"M. Strüber, P. M. Jonas, and M. Bartos, “Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells,” <i>PNAS</i>, vol. 112, no. 4. National Academy of Sciences, pp. 1220–1225, 2015.","chicago":"Strüber, Michael, Peter M Jonas, and Marlene Bartos. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” <i>PNAS</i>. National Academy of Sciences, 2015. <a href=\"https://doi.org/10.1073/pnas.1412996112\">https://doi.org/10.1073/pnas.1412996112</a>.","short":"M. Strüber, P.M. Jonas, M. Bartos, PNAS 112 (2015) 1220–1225.","ista":"Strüber M, Jonas PM, Bartos M. 2015. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. PNAS. 112(4), 1220–1225.","ama":"Strüber M, Jonas PM, Bartos M. Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. <i>PNAS</i>. 2015;112(4):1220-1225. doi:<a href=\"https://doi.org/10.1073/pnas.1412996112\">10.1073/pnas.1412996112</a>","mla":"Strüber, Michael, et al. “Strength and Duration of Perisomatic GABAergic Inhibition Depend on Distance between Synaptically Connected Cells.” <i>PNAS</i>, vol. 112, no. 4, National Academy of Sciences, 2015, pp. 1220–25, doi:<a href=\"https://doi.org/10.1073/pnas.1412996112\">10.1073/pnas.1412996112</a>.","apa":"Strüber, M., Jonas, P. M., &#38; Bartos, M. (2015). Strength and duration of perisomatic GABAergic inhibition depend on distance between synaptically connected cells. <i>PNAS</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.1412996112\">https://doi.org/10.1073/pnas.1412996112</a>"},"oa":1,"day":"27","volume":112,"oa_version":"Published Version","page":"1220 - 1225","file":[{"date_created":"2019-01-17T07:52:40Z","date_updated":"2020-07-14T12:45:07Z","access_level":"open_access","checksum":"6703309a1f58493cf5a704211fb6ebed","file_size":1280860,"content_type":"application/pdf","relation":"main_file","file_name":"2015_PNAS_Strueber.pdf","file_id":"5838","creator":"dernst"}]},{"date_updated":"2021-01-12T06:53:52Z","type":"journal_article","intvolume":"        51","publication_status":"published","month":"02","language":[{"iso":"eng"}],"year":"2014","doi":"10.1111/psyp.12062","ddc":["000"],"date_created":"2018-12-11T11:54:34Z","_id":"1890","scopus_import":1,"date_published":"2014-02-11T00:00:00Z","pubrep_id":"442","abstract":[{"text":"To search for a target in a complex environment is an everyday behavior that ends with finding the target. When we search for two identical targets, however, we must continue the search after finding the first target and memorize its location. We used fixation-related potentials to investigate the neural correlates of different stages of the search, that is, before and after finding the first target. Having found the first target influenced subsequent distractor processing. Compared to distractor fixations before the first target fixation, a negative shift was observed for three subsequent distractor fixations. These results suggest that processing a target in continued search modulates the brain's response, either transiently by reflecting temporary working memory processes or permanently by reflecting working memory retention.","lang":"eng"}],"author":[{"full_name":"Körner, Christof","first_name":"Christof","last_name":"Körner"},{"first_name":"Verena","last_name":"Braunstein","full_name":"Braunstein, Verena"},{"full_name":"Stangl, Matthias","first_name":"Matthias","last_name":"Stangl"},{"id":"45BF87EE-F248-11E8-B48F-1D18A9856A87","first_name":"Alois","orcid":"0000-0002-5621-8100","last_name":"Schlögl","full_name":"Schlögl, Alois"},{"first_name":"Christa","last_name":"Neuper","full_name":"Neuper, Christa"},{"full_name":"Ischebeck, Anja","first_name":"Anja","last_name":"Ischebeck"}],"issue":"4","publisher":"Wiley-Blackwell","has_accepted_license":"1","title":"Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection","department":[{"_id":"ScienComp"},{"_id":"PeJo"}],"status":"public","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","file_date_updated":"2020-07-14T12:45:20Z","publication":"Psychophysiology","publist_id":"5205","acknowledgement":"Funded by Austrian Science Fund (FWF) Grant Number: P 22189-B18; European Union within the 6th Framework Programme Grant Number: 517590; State government of Styria Grant Number: PN 4055","file":[{"access_level":"open_access","checksum":"4255b6185e774acce1d99f8e195c564d","date_created":"2018-12-12T10:16:44Z","date_updated":"2020-07-14T12:45:20Z","file_name":"IST-2016-442-v1+1_K-rner_et_al-2014-Psychophysiology.pdf","content_type":"application/pdf","relation":"main_file","file_id":"5233","creator":"system","file_size":543243}],"page":"385 - 395","oa_version":"Published Version","volume":51,"tmp":{"image":"/images/cc_by.png","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)"},"day":"11","citation":{"short":"C. Körner, V. Braunstein, M. Stangl, A. Schlögl, C. Neuper, A. Ischebeck, Psychophysiology 51 (2014) 385–395.","chicago":"Körner, Christof, Verena Braunstein, Matthias Stangl, Alois Schlögl, Christa Neuper, and Anja Ischebeck. “Sequential Effects in Continued Visual Search: Using Fixation-Related Potentials to Compare Distractor Processing before and after Target Detection.” <i>Psychophysiology</i>. Wiley-Blackwell, 2014. <a href=\"https://doi.org/10.1111/psyp.12062\">https://doi.org/10.1111/psyp.12062</a>.","ieee":"C. Körner, V. Braunstein, M. Stangl, A. Schlögl, C. Neuper, and A. Ischebeck, “Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection,” <i>Psychophysiology</i>, vol. 51, no. 4. Wiley-Blackwell, pp. 385–395, 2014.","apa":"Körner, C., Braunstein, V., Stangl, M., Schlögl, A., Neuper, C., &#38; Ischebeck, A. (2014). Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. <i>Psychophysiology</i>. Wiley-Blackwell. <a href=\"https://doi.org/10.1111/psyp.12062\">https://doi.org/10.1111/psyp.12062</a>","mla":"Körner, Christof, et al. “Sequential Effects in Continued Visual Search: Using Fixation-Related Potentials to Compare Distractor Processing before and after Target Detection.” <i>Psychophysiology</i>, vol. 51, no. 4, Wiley-Blackwell, 2014, pp. 385–95, doi:<a href=\"https://doi.org/10.1111/psyp.12062\">10.1111/psyp.12062</a>.","ama":"Körner C, Braunstein V, Stangl M, Schlögl A, Neuper C, Ischebeck A. Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. <i>Psychophysiology</i>. 2014;51(4):385-395. doi:<a href=\"https://doi.org/10.1111/psyp.12062\">10.1111/psyp.12062</a>","ista":"Körner C, Braunstein V, Stangl M, Schlögl A, Neuper C, Ischebeck A. 2014. Sequential effects in continued visual search: Using fixation-related potentials to compare distractor processing before and after target detection. Psychophysiology. 51(4), 385–395."},"oa":1},{"publisher":"Public Library of Science","has_accepted_license":"1","title":"Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus","department":[{"_id":"PeJo"}],"status":"public","file_date_updated":"2020-07-14T12:45:24Z","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","publication":"PLoS One","publist_id":"5074","project":[{"_id":"25C0F108-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"268548","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"}],"file":[{"checksum":"85e4f4ea144f827272aaf376b2830564","access_level":"open_access","date_updated":"2020-07-14T12:45:24Z","date_created":"2018-12-12T10:14:52Z","creator":"system","file_id":"5107","file_name":"IST-2016-434-v1+1_journal.pone.0113124.pdf","relation":"main_file","content_type":"application/pdf","file_size":5179993}],"oa_version":"Published Version","volume":9,"tmp":{"image":"/images/cc_by_sa.png","name":"Creative Commons Attribution-ShareAlike 4.0 International Public License (CC BY-SA 4.0)","legal_code_url":"https://creativecommons.org/licenses/by-sa/4.0/legalcode","short":"CC BY-SA (4.0)"},"article_number":"0113124","day":"19","oa":1,"citation":{"apa":"Kim, S. (2014). Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. <i>PLoS One</i>. Public Library of Science. <a href=\"https://doi.org/10.1371/journal.pone.0113124\">https://doi.org/10.1371/journal.pone.0113124</a>","ama":"Kim S. Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. <i>PLoS One</i>. 2014;9(11). doi:<a href=\"https://doi.org/10.1371/journal.pone.0113124\">10.1371/journal.pone.0113124</a>","mla":"Kim, Sooyun. “Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus.” <i>PLoS One</i>, vol. 9, no. 11, 0113124, Public Library of Science, 2014, doi:<a href=\"https://doi.org/10.1371/journal.pone.0113124\">10.1371/journal.pone.0113124</a>.","ista":"Kim S. 2014. Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus. PLoS One. 9(11), 0113124.","short":"S. Kim, PLoS One 9 (2014).","ieee":"S. Kim, “Action potential modulation in CA1 pyramidal neuron axons facilitates OLM interneuron activation in recurrent inhibitory microcircuits of rat hippocampus,” <i>PLoS One</i>, vol. 9, no. 11. Public Library of Science, 2014.","chicago":"Kim, Sooyun. “Action Potential Modulation in CA1 Pyramidal Neuron Axons Facilitates OLM Interneuron Activation in Recurrent Inhibitory Microcircuits of Rat Hippocampus.” <i>PLoS One</i>. Public Library of Science, 2014. <a href=\"https://doi.org/10.1371/journal.pone.0113124\">https://doi.org/10.1371/journal.pone.0113124</a>."},"quality_controlled":"1","type":"journal_article","date_updated":"2021-01-12T06:54:39Z","publication_status":"published","intvolume":"         9","month":"11","language":[{"iso":"eng"}],"doi":"10.1371/journal.pone.0113124","year":"2014","ddc":["570"],"date_created":"2018-12-11T11:55:09Z","_id":"2002","date_published":"2014-11-19T00:00:00Z","scopus_import":1,"license":"https://creativecommons.org/licenses/by-sa/4.0/","pubrep_id":"434","author":[{"id":"394AB1C8-F248-11E8-B48F-1D18A9856A87","full_name":"Kim, Sooyun","last_name":"Kim","first_name":"Sooyun"}],"ec_funded":1,"abstract":[{"lang":"eng","text":"Oriens-lacunosum moleculare (O-LM) interneurons in the CA1 region of the hippocampus play a key role in feedback inhibition and in the control of network activity. However, how these cells are efficiently activated in the network remains unclear. To address this question, I performed recordings from CA1 pyramidal neuron axons, the presynaptic fibers that provide feedback innervation of these interneurons. Two forms of axonal action potential (AP) modulation were identified. First, repetitive stimulation resulted in activity-dependent AP broadening. Broadening showed fast onset, with marked changes in AP shape following a single AP. Second, tonic depolarization in CA1 pyramidal neuron somata induced AP broadening in the axon, and depolarization-induced broadening summated with activity-dependent broadening. Outsideout patch recordings from CA1 pyramidal neuron axons revealed a high density of a-dendrotoxin (α-DTX)-sensitive, inactivating K+ channels, suggesting that K+ channel inactivation mechanistically contributes to AP broadening. To examine the functional consequences of axonal AP modulation for synaptic transmission, I performed paired recordings between synaptically connected CA1 pyramidal neurons and O-LM interneurons. CA1 pyramidal neuron-O-LM interneuron excitatory postsynaptic currents (EPSCs) showed facilitation during both repetitive stimulation and tonic depolarization of the presynaptic neuron. Both effects were mimicked and occluded by α-DTX, suggesting that they were mediated by K+ channel inactivation. Therefore, axonal AP modulation can greatly facilitate the activation of O-LM interneurons. In conclusion, modulation of AP shape in CA1 pyramidal neuron axons substantially enhances the efficacy of principal neuron-interneuron synapses, promoting the activation of O-LM interneurons in recurrent inhibitory microcircuits."}],"issue":"11"},{"project":[{"name":"Mechanisms of transmitter release at GABAergic synapses","grant_number":"P24909-B24","call_identifier":"FWF","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"},{"grant_number":"268548","call_identifier":"FP7","_id":"25C0F108-B435-11E9-9278-68D0E5697425","name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons"}],"publist_id":"5041","publication":"eLife","file_date_updated":"2020-07-14T12:45:26Z","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","title":"Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse","department":[{"_id":"PeJo"}],"status":"public","has_accepted_license":"1","publisher":"eLife Sciences Publications","quality_controlled":"1","oa":1,"citation":{"short":"itaru Arai, P.M. Jonas, ELife 3 (2014).","ieee":"itaru Arai and P. M. Jonas, “Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse,” <i>eLife</i>, vol. 3. eLife Sciences Publications, 2014.","chicago":"Arai, itaru, and Peter M Jonas. “Nanodomain Coupling Explains Ca^2+ Independence of Transmitter Release Time Course at a Fast Central Synapse.” <i>ELife</i>. eLife Sciences Publications, 2014. <a href=\"https://doi.org/10.7554/eLife.04057\">https://doi.org/10.7554/eLife.04057</a>.","mla":"Arai, itaru, and Peter M. Jonas. “Nanodomain Coupling Explains Ca^2+ Independence of Transmitter Release Time Course at a Fast Central Synapse.” <i>ELife</i>, vol. 3, eLife Sciences Publications, 2014, doi:<a href=\"https://doi.org/10.7554/eLife.04057\">10.7554/eLife.04057</a>.","ama":"Arai  itaru, Jonas PM. Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. <i>eLife</i>. 2014;3. doi:<a href=\"https://doi.org/10.7554/eLife.04057\">10.7554/eLife.04057</a>","apa":"Arai,  itaru, &#38; Jonas, P. M. (2014). Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. <i>ELife</i>. eLife Sciences Publications. <a href=\"https://doi.org/10.7554/eLife.04057\">https://doi.org/10.7554/eLife.04057</a>","ista":"Arai  itaru, Jonas PM. 2014. Nanodomain coupling explains Ca^2+ independence of transmitter release time course at a fast central synapse. eLife. 3."},"day":"09","oa_version":"Submitted Version","volume":3,"file":[{"file_size":2239563,"relation":"main_file","content_type":"application/pdf","file_name":"IST-2016-421-v1+1_e04057.full.pdf","creator":"system","file_id":"5094","date_created":"2018-12-12T10:14:41Z","date_updated":"2020-07-14T12:45:26Z","checksum":"c240f915450d4ebe8f95043a2a8c7b1a","access_level":"open_access"}],"ddc":["570"],"doi":"10.7554/eLife.04057","year":"2014","language":[{"iso":"eng"}],"month":"12","publication_status":"published","intvolume":"         3","type":"journal_article","date_updated":"2021-01-12T06:54:51Z","abstract":[{"text":"A puzzling property of synaptic transmission, originally established at the neuromuscular junction, is that the time course of transmitter release is independent of the extracellular Ca2+ concentration ([Ca2+]o), whereas the rate of release is highly [Ca2+]o-dependent. Here, we examine the time course of release at inhibitory basket cell-Purkinje cell synapses and show that it is independent of [Ca2+]o. Modeling of Ca2+-dependent transmitter release suggests that the invariant time course of release critically depends on tight coupling between Ca2+ channels and release sensors. Experiments with exogenous Ca2+ chelators reveal that channel-sensor coupling at basket cell-Purkinje cell synapses is very tight, with a mean distance of 10–20 nm. Thus, tight channel-sensor coupling provides a mechanistic explanation for the apparent [Ca2+]o independence of the time course of release.","lang":"eng"}],"ec_funded":1,"author":[{"id":"32A73F6C-F248-11E8-B48F-1D18A9856A87","last_name":"Arai","first_name":"Itaru","full_name":"Arai, Itaru"},{"full_name":"Jonas, Peter M","first_name":"Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"pubrep_id":"421","date_published":"2014-12-09T00:00:00Z","scopus_import":1,"_id":"2031","date_created":"2018-12-11T11:55:19Z"},{"date_published":"2014-09-10T00:00:00Z","scopus_import":1,"_id":"2041","date_created":"2018-12-11T11:55:22Z","author":[{"full_name":"Jonas, Peter M","last_name":"Jonas","orcid":"0000-0001-5001-4804","first_name":"Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"},{"first_name":"John","last_name":"Lisman","full_name":"Lisman, John"}],"abstract":[{"text":"The hippocampus mediates several higher brain functions, such as learning, memory, and spatial coding. The input region of the hippocampus, the dentate gyrus, plays a critical role in these processes. Several lines of evidence suggest that the dentate gyrus acts as a preprocessor of incoming information, preparing it for subsequent processing in CA3. For example, the dentate gyrus converts input from the entorhinal cortex, where cells have multiple spatial fields, into the spatially more specific place cell activity characteristic of the CA3 region. Furthermore, the dentate gyrus is involved in pattern separation, transforming relatively similar input patterns into substantially different output patterns. Finally, the dentate gyrus produces a very sparse coding scheme in which only a very small fraction of neurons are active at any one time.","lang":"eng"}],"pubrep_id":"424","publication_status":"published","intvolume":"         8","type":"journal_article","date_updated":"2021-01-12T06:54:55Z","ddc":["570"],"doi":"10.3389/fncir.2014.00107","year":"2014","language":[{"iso":"eng"}],"month":"09","tmp":{"image":"/images/cc_by.png","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)"},"oa_version":"Published Version","volume":8,"file":[{"access_level":"open_access","checksum":"3ca57b164045523f876407e9f13a9fb8","date_created":"2018-12-12T10:17:38Z","date_updated":"2020-07-14T12:45:26Z","file_name":"IST-2016-424-v1+1_fncir-08-00107.pdf","relation":"main_file","content_type":"application/pdf","file_id":"5294","creator":"system","file_size":201110}],"quality_controlled":"1","oa":1,"citation":{"apa":"Jonas, P. M., &#38; Lisman, J. (2014). Structure, function and plasticity of hippocampal dentate gyrus microcircuits. <i>Frontiers in Neural Circuits</i>. Frontiers Research Foundation. <a href=\"https://doi.org/10.3389/fncir.2014.00107\">https://doi.org/10.3389/fncir.2014.00107</a>","ama":"Jonas PM, Lisman J. Structure, function and plasticity of hippocampal dentate gyrus microcircuits. <i>Frontiers in Neural Circuits</i>. 2014;8. doi:<a href=\"https://doi.org/10.3389/fncir.2014.00107\">10.3389/fncir.2014.00107</a>","mla":"Jonas, Peter M., and John Lisman. “Structure, Function and Plasticity of Hippocampal Dentate Gyrus Microcircuits.” <i>Frontiers in Neural Circuits</i>, vol. 8, 2p, Frontiers Research Foundation, 2014, doi:<a href=\"https://doi.org/10.3389/fncir.2014.00107\">10.3389/fncir.2014.00107</a>.","ista":"Jonas PM, Lisman J. 2014. Structure, function and plasticity of hippocampal dentate gyrus microcircuits. Frontiers in Neural Circuits. 8, 2p.","short":"P.M. Jonas, J. Lisman, Frontiers in Neural Circuits 8 (2014).","chicago":"Jonas, Peter M, and John Lisman. “Structure, Function and Plasticity of Hippocampal Dentate Gyrus Microcircuits.” <i>Frontiers in Neural Circuits</i>. Frontiers Research Foundation, 2014. <a href=\"https://doi.org/10.3389/fncir.2014.00107\">https://doi.org/10.3389/fncir.2014.00107</a>.","ieee":"P. M. Jonas and J. Lisman, “Structure, function and plasticity of hippocampal dentate gyrus microcircuits,” <i>Frontiers in Neural Circuits</i>, vol. 8. Frontiers Research Foundation, 2014."},"article_number":"2p","day":"10","file_date_updated":"2020-07-14T12:45:26Z","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","department":[{"_id":"PeJo"}],"title":"Structure, function and plasticity of hippocampal dentate gyrus microcircuits","status":"public","has_accepted_license":"1","publisher":"Frontiers Research Foundation","publist_id":"5010","publication":"Frontiers in Neural Circuits"},{"quality_controlled":"1","citation":{"ista":"Hu H, Gan J, Jonas PM. 2014. Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. Science. 345(6196), 1255263.","ama":"Hu H, Gan J, Jonas PM. Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. <i>Science</i>. 2014;345(6196). doi:<a href=\"https://doi.org/10.1126/science.1255263\">10.1126/science.1255263</a>","mla":"Hu, Hua, et al. “Fast-Spiking Parvalbumin^+ GABAergic Interneurons: From Cellular Design to Microcircuit Function.” <i>Science</i>, vol. 345, no. 6196, 1255263, American Association for the Advancement of Science, 2014, doi:<a href=\"https://doi.org/10.1126/science.1255263\">10.1126/science.1255263</a>.","apa":"Hu, H., Gan, J., &#38; Jonas, P. M. (2014). Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function. <i>Science</i>. American Association for the Advancement of Science. <a href=\"https://doi.org/10.1126/science.1255263\">https://doi.org/10.1126/science.1255263</a>","chicago":"Hu, Hua, Jian Gan, and Peter M Jonas. “Fast-Spiking Parvalbumin^+ GABAergic Interneurons: From Cellular Design to Microcircuit Function.” <i>Science</i>. American Association for the Advancement of Science, 2014. <a href=\"https://doi.org/10.1126/science.1255263\">https://doi.org/10.1126/science.1255263</a>.","ieee":"H. Hu, J. Gan, and P. M. Jonas, “Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function,” <i>Science</i>, vol. 345, no. 6196. American Association for the Advancement of Science, 2014.","short":"H. Hu, J. Gan, P.M. Jonas, Science 345 (2014)."},"oa":1,"day":"01","article_number":"1255263","oa_version":"Submitted Version","volume":345,"file":[{"file_id":"5185","creator":"system","relation":"main_file","content_type":"application/pdf","file_name":"IST-2017-821-v1+1_1255263JonasPVReviewTextR_Final.pdf","file_size":215514,"access_level":"open_access","checksum":"a0036a589037d37e86364fa25cc0a82f","date_updated":"2020-07-14T12:45:27Z","date_created":"2018-12-12T10:16:00Z"},{"date_created":"2018-12-12T10:16:01Z","date_updated":"2020-07-14T12:45:27Z","access_level":"open_access","checksum":"e1f57d2713725449cb898fdcb8ef47b8","file_size":1732723,"file_name":"IST-2017-821-v1+2_1255263JonasPVReviewFigures_Final.pdf","relation":"main_file","content_type":"application/pdf","file_id":"5186","creator":"system"}],"project":[{"name":"Mechanisms of transmitter release at GABAergic synapses","call_identifier":"FWF","grant_number":"P24909-B24","_id":"25C26B1E-B435-11E9-9278-68D0E5697425"},{"name":"Nanophysiology of fast-spiking, parvalbumin-expressing GABAergic interneurons","_id":"25C0F108-B435-11E9-9278-68D0E5697425","call_identifier":"FP7","grant_number":"268548"}],"publist_id":"4984","publication":"Science","user_id":"4435EBFC-F248-11E8-B48F-1D18A9856A87","file_date_updated":"2020-07-14T12:45:27Z","status":"public","department":[{"_id":"PeJo"}],"title":"Fast-spiking parvalbumin^+ GABAergic interneurons: From cellular design to microcircuit function","has_accepted_license":"1","publisher":"American Association for the Advancement of Science","issue":"6196","abstract":[{"text":"The success story of fast-spiking, parvalbumin-positive (PV+) GABAergic interneurons (GABA, γ-aminobutyric acid) in the mammalian central nervous system is noteworthy. In 1995, the properties of these interneurons were completely unknown. Twenty years later, thanks to the massive use of subcellular patch-clamp techniques, simultaneous multiple-cell recording, optogenetics, in vivo measurements, and computational approaches, our knowledge about PV+ interneurons became more extensive than for several types of pyramidal neurons. These findings have implications beyond the “small world” of basic research on GABAergic cells. For example, the results provide a first proof of principle that neuroscientists might be able to close the gaps between the molecular, cellular, network, and behavioral levels, representing one of the main challenges at the present time. Furthermore, the results may form the basis for PV+ interneurons as therapeutic targets for brain disease in the future. However, much needs to be learned about the basic function of these interneurons before clinical neuroscientists will be able to use PV+ interneurons for therapeutic purposes.","lang":"eng"}],"author":[{"first_name":"Hua","last_name":"Hu","full_name":"Hu, Hua","id":"4AC0145C-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Gan, Jian","first_name":"Jian","last_name":"Gan","id":"3614E438-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Jonas, Peter M","first_name":"Peter M","orcid":"0000-0001-5001-4804","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87"}],"ec_funded":1,"pubrep_id":"821","scopus_import":1,"date_published":"2014-08-01T00:00:00Z","_id":"2062","date_created":"2018-12-11T11:55:29Z","ddc":["570"],"year":"2014","doi":"10.1126/science.1255263","language":[{"iso":"eng"}],"month":"08","intvolume":"       345","publication_status":"published","date_updated":"2021-01-12T06:55:03Z","type":"journal_article"}]