{"date_created":"2018-12-11T12:05:23Z","date_published":"2008-01-01T00:00:00Z","type":"journal_article","publisher":"National Academy of Sciences","volume":105,"year":"2008","day":"01","month":"01","status":"public","title":"Differential dependence of phasic transmitter release on synaptotagmin 1 at GABAergic and glutamatergic hippocampal synapses","publication_status":"published","extern":1,"page":"15581 - 6","issue":"40","doi":"10.1073/pnas.0800621105","publist_id":"2384","author":[{"full_name":"Kerr, Angharad M","last_name":"Kerr","first_name":"Angharad"},{"last_name":"Reisinger","full_name":"Reisinger, Ellen","first_name":"Ellen"},{"last_name":"Jonas","full_name":"Peter Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804","first_name":"Peter M"}],"intvolume":"       105","citation":{"chicago":"Kerr, Angharad, Ellen Reisinger, and Peter M Jonas. “Differential Dependence of Phasic Transmitter Release on Synaptotagmin 1 at GABAergic and Glutamatergic Hippocampal Synapses.” <i>PNAS</i>. National Academy of Sciences, 2008. <a href=\"https://doi.org/10.1073/pnas.0800621105\">https://doi.org/10.1073/pnas.0800621105</a>.","apa":"Kerr, A., Reisinger, E., &#38; Jonas, P. M. (2008). Differential dependence of phasic transmitter release on synaptotagmin 1 at GABAergic and glutamatergic hippocampal synapses. <i>PNAS</i>. National Academy of Sciences. <a href=\"https://doi.org/10.1073/pnas.0800621105\">https://doi.org/10.1073/pnas.0800621105</a>","mla":"Kerr, Angharad, et al. “Differential Dependence of Phasic Transmitter Release on Synaptotagmin 1 at GABAergic and Glutamatergic Hippocampal Synapses.” <i>PNAS</i>, vol. 105, no. 40, National Academy of Sciences, 2008, pp. 15581–86, doi:<a href=\"https://doi.org/10.1073/pnas.0800621105\">10.1073/pnas.0800621105</a>.","ieee":"A. Kerr, E. Reisinger, and P. M. Jonas, “Differential dependence of phasic transmitter release on synaptotagmin 1 at GABAergic and glutamatergic hippocampal synapses,” <i>PNAS</i>, vol. 105, no. 40. National Academy of Sciences, pp. 15581–6, 2008.","ista":"Kerr A, Reisinger E, Jonas PM. 2008. Differential dependence of phasic transmitter release on synaptotagmin 1 at GABAergic and glutamatergic hippocampal synapses. PNAS. 105(40), 15581–6.","ama":"Kerr A, Reisinger E, Jonas PM. Differential dependence of phasic transmitter release on synaptotagmin 1 at GABAergic and glutamatergic hippocampal synapses. <i>PNAS</i>. 2008;105(40):15581-15586. doi:<a href=\"https://doi.org/10.1073/pnas.0800621105\">10.1073/pnas.0800621105</a>","short":"A. Kerr, E. Reisinger, P.M. Jonas, PNAS 105 (2008) 15581–6."},"publication":"PNAS","_id":"3827","abstract":[{"lang":"eng","text":"Previous studies revealed that synaptotagmin 1 is the major Ca(2+) sensor for fast synchronous transmitter release at excitatory synapses. However, the molecular identity of the Ca(2+) sensor at hippocampal inhibitory synapses has not been determined. To address the functional role of synaptotagmin 1 at identified inhibitory terminals, we made paired recordings from synaptically connected basket cells (BCs) and granule cells (GCs) in the dentate gyrus in organotypic slice cultures from wild-type and synaptotagmin 1-deficient mice. As expected, genetic elimination of synaptotagmin 1 abolished synchronous transmitter release at excitatory GC-BC synapses. However, synchronous release at inhibitory BC-GC synapses was maintained. Quantitative analysis revealed that elimination of synaptotagmin 1 reduced release probability and depression but maintained the synchrony of transmitter release at BC-GC synapses. Elimination of synaptotagmin 1 also increased the frequency of both miniature excitatory postsynaptic currents (measured in BCs) and miniature inhibitory postsynaptic currents (recorded in GCs), consistent with a clamping function of synaptotagmin 1 at both excitatory and inhibitory terminals. Single-cell reverse-transcription quantitative PCR analysis revealed that single BCs coexpressed multiple synaptotagmin isoforms, including synaptotagmin 1-5, 7, and 11-13. Our results indicate that, in contrast to excitatory synapses, synaptotagmin 1 is not absolutely required for synchronous release at inhibitory BC-GC synapses. Thus, alternative fast Ca(2+) sensors contribute to synchronous release of the inhibitory transmitter GABA in cortical circuits."}],"date_updated":"2021-01-12T07:52:29Z","quality_controlled":0}