{"language":[{"iso":"eng"}],"_id":"2969","citation":{"short":"S. Goswami, I. Bucurenciu, P.M. Jonas, Journal of Neuroscience 32 (2012) 14294–14304.","ista":"Goswami S, Bucurenciu I, Jonas PM. 2012. Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. Journal of Neuroscience. 32(41), 14294–14304.","apa":"Goswami, S., Bucurenciu, I., &#38; Jonas, P. M. (2012). Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. <i>Journal of Neuroscience</i>. Society for Neuroscience. <a href=\"https://doi.org/10.1523/JNEUROSCI.6104-11.2012\">https://doi.org/10.1523/JNEUROSCI.6104-11.2012</a>","chicago":"Goswami, Sarit, Iancu Bucurenciu, and Peter M Jonas. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” <i>Journal of Neuroscience</i>. Society for Neuroscience, 2012. <a href=\"https://doi.org/10.1523/JNEUROSCI.6104-11.2012\">https://doi.org/10.1523/JNEUROSCI.6104-11.2012</a>.","ama":"Goswami S, Bucurenciu I, Jonas PM. Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling. <i>Journal of Neuroscience</i>. 2012;32(41):14294-14304. doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.6104-11.2012\">10.1523/JNEUROSCI.6104-11.2012</a>","ieee":"S. Goswami, I. Bucurenciu, and P. M. Jonas, “Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling,” <i>Journal of Neuroscience</i>, vol. 32, no. 41. Society for Neuroscience, pp. 14294–14304, 2012.","mla":"Goswami, Sarit, et al. “Miniature IPSCs in Hippocampal Granule Cells Are Triggered by Voltage-Gated Ca^(2+) Channels via Microdomain Coupling.” <i>Journal of Neuroscience</i>, vol. 32, no. 41, Society for Neuroscience, 2012, pp. 14294–304, doi:<a href=\"https://doi.org/10.1523/JNEUROSCI.6104-11.2012\">10.1523/JNEUROSCI.6104-11.2012</a>."},"external_id":{"pmid":["23055500"]},"doi":"10.1523/JNEUROSCI.6104-11.2012","page":"14294 - 14304","publication":"Journal of Neuroscience","author":[{"first_name":"Sarit","last_name":"Goswami","full_name":"Goswami, Sarit","id":"3A578F32-F248-11E8-B48F-1D18A9856A87"},{"full_name":"Bucurenciu, Iancu","first_name":"Iancu","last_name":"Bucurenciu"},{"first_name":"Peter M","last_name":"Jonas","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","full_name":"Jonas, Peter M","orcid":"0000-0001-5001-4804"}],"project":[{"_id":"25BDE9A4-B435-11E9-9278-68D0E5697425","name":"Glutamaterge synaptische Übertragung und Plastizität in hippocampalen Mikroschaltkreisen","grant_number":"SFB-TR3-TP10B"}],"acknowledgement":"This work was supported by grants from the Deutsche Forschungsgemeinschaft (TR 3/B10, Leibniz program, GSC-4 Spemann Graduate School) and the European Union (European Research Council Advanced Grant).","year":"2012","publist_id":"3744","volume":32,"intvolume":"        32","abstract":[{"lang":"eng","text":"The coupling between presynaptic Ca^(2+) channels and Ca^(2+) sensors of exocytosis is a key determinant of synaptic transmission. Evoked release from parvalbumin (PV)-expressing interneurons is triggered by nanodomain coupling of P/Q-type Ca^(2+) channels, whereas release from cholecystokinin (CCK)-containing interneurons is generated by microdomain coupling of N-type channels. Nanodomain coupling has several functional advantages, including speed and efficacy of transmission. One potential disadvantage is that stochastic\r\nopening of presynaptic Ca^(2+) channels may trigger spontaneous transmitter release. We addressed this possibility in rat hippocampal\r\ngranule cells, which receive converging inputs from different inhibitory sources. Both reduction of extracellular Ca^(2+) concentration and the unselective Ca^(2+) channel blocker Cd^(2+) reduced the frequency of miniature IPSCs (mIPSCs) in granule cells by ~50%, suggesting that the opening of presynaptic Ca^(2+) channels contributes to spontaneous release. Application of the selective P/Q-type Ca^(2+) channel blocker\r\nω-agatoxin IVa had no detectable effects, whereas both the N-type blocker ω-conotoxin GVIa and the L-type blocker nimodipine reduced\r\nmIPSC frequency. Furthermore, both the fast Ca^(2+) chelator BAPTA-AM and the slow chelator EGTA-AM reduced the mIPSC frequency,\r\nsuggesting that Ca^(2+)-dependent spontaneous release is triggered by microdomain rather than nanodomain coupling. The CB_(1) receptor\r\nagonist WIN 55212-2 also decreased spontaneous release; this effect was occluded by prior application of ω-conotoxin GVIa, suggesting that a major fraction of Ca^(2+)-dependent spontaneous release was generated at the terminals of CCK-expressing interneurons. Tonic inhibition generated by spontaneous opening of presynaptic N- and L-type Ca^(2+) channels may be important for hippocampal information processing.\r\n"}],"main_file_link":[{"open_access":"1","url":"http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3632771/"}],"department":[{"_id":"PeJo"}],"issue":"41","publication_status":"published","date_published":"2012-10-10T00:00:00Z","date_updated":"2021-01-12T07:40:08Z","pmid":1,"month":"10","day":"10","type":"journal_article","status":"public","title":"Miniature IPSCs in hippocampal granule cells are triggered by voltage-gated Ca^(2+) channels via microdomain coupling","quality_controlled":"1","scopus_import":1,"publisher":"Society for Neuroscience","user_id":"3E5EF7F0-F248-11E8-B48F-1D18A9856A87","date_created":"2018-12-11T12:00:36Z","oa":1,"oa_version":"Submitted Version"}