{"isi":1,"year":"2017","intvolume":"        94","volume":94,"publist_id":"6408","language":[{"iso":"eng"}],"_id":"991","citation":{"ista":"Chen C, Jonas PM. 2017. Synaptotagmins: That’s why so many. Neuron. 94(4), 694–696.","apa":"Chen, C., &#38; Jonas, P. M. (2017). Synaptotagmins: That’s why so many. <i>Neuron</i>. Elsevier. <a href=\"https://doi.org/10.1016/j.neuron.2017.05.011\">https://doi.org/10.1016/j.neuron.2017.05.011</a>","chicago":"Chen, Chong, and Peter M Jonas. “Synaptotagmins: That’s Why so Many.” <i>Neuron</i>. Elsevier, 2017. <a href=\"https://doi.org/10.1016/j.neuron.2017.05.011\">https://doi.org/10.1016/j.neuron.2017.05.011</a>.","ama":"Chen C, Jonas PM. Synaptotagmins: That’s why so many. <i>Neuron</i>. 2017;94(4):694-696. doi:<a href=\"https://doi.org/10.1016/j.neuron.2017.05.011\">10.1016/j.neuron.2017.05.011</a>","short":"C. Chen, P.M. Jonas, Neuron 94 (2017) 694–696.","mla":"Chen, Chong, and Peter M. Jonas. “Synaptotagmins: That’s Why so Many.” <i>Neuron</i>, vol. 94, no. 4, Elsevier, 2017, pp. 694–96, doi:<a href=\"https://doi.org/10.1016/j.neuron.2017.05.011\">10.1016/j.neuron.2017.05.011</a>.","ieee":"C. Chen and P. M. Jonas, “Synaptotagmins: That’s why so many,” <i>Neuron</i>, vol. 94, no. 4. Elsevier, pp. 694–696, 2017."},"external_id":{"isi":["000401415100002"]},"publication_identifier":{"issn":["08966273"]},"doi":"10.1016/j.neuron.2017.05.011","page":"694 - 696","author":[{"full_name":"Chen, Chong","id":"3DFD581A-F248-11E8-B48F-1D18A9856A87","last_name":"Chen","first_name":"Chong"},{"last_name":"Jonas","first_name":"Peter M","full_name":"Jonas, Peter M","id":"353C1B58-F248-11E8-B48F-1D18A9856A87","orcid":"0000-0001-5001-4804"}],"publication":"Neuron","quality_controlled":"1","title":"Synaptotagmins: That’s why so many","status":"public","publisher":"Elsevier","scopus_import":"1","oa_version":"None","user_id":"c635000d-4b10-11ee-a964-aac5a93f6ac1","date_created":"2018-12-11T11:49:34Z","department":[{"_id":"PeJo"}],"abstract":[{"text":"Synaptotagmin 7 (Syt7) was originally identified as a slow Ca2+ sensor for lysosome fusion, but its function at fast synapses is controversial. The paper by Luo and Südhof (2017) in this issue of Neuron shows that at the calyx of Held in the auditory brainstem Syt7 triggers asynchronous release during stimulus trains, resulting in reliable and temporally precise high-frequency transmission. Thus, a slow Ca2+ sensor contributes to the fast signaling properties of the calyx synapse.","lang":"eng"}],"date_published":"2017-05-17T00:00:00Z","publication_status":"published","issue":"4","article_processing_charge":"No","month":"05","date_updated":"2023-09-22T09:54:37Z","type":"journal_article","day":"17"}