{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T01:20:12Z","timestamp":1789953612514,"version":"4.0.1"},"reference-count":0,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[1996,12,15]],"date-time":"1996-12-15T00:00:00Z","timestamp":850608000000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1996,12,15]]},"abstract":"<jats:p>1. The involvement of the different types of voltage\u2010dependent calcium channels (VDCCs) in synaptic transmission at the mature and newly formed mammalian neuromuscular junction was studied by evaluating the effects of L\u2010, P\/Q\u2010 and N\u2010type VDCC antagonists on transmitter release in normal and reinnervating levator auris preparations of adult mice. 2. Nerve\u2010evoked transmitter release was blocked by omega\u2010agatoxin IVA (omega\u2010AgaIVA), a P\/Q\u2010type VDCC blocker, both in normal and reinnervating endplates (100 nM omega\u2010AgaIVA caused &gt; 90% inhibition). The N\u2010type VDCC antagonist omega\u2010conotoxin GVIA (omega\u2010CgTX; 1 and 5 microM), as occurs in normal preparations, did not significantly affect this type of release during reinnervation. Nitrendipine (1\u201010 microM), an L\u2010type VDCC blocker, strongly antagonized release in reinnervating muscles (approximately 40\u201069% blockade) and lacked any effect in normal preparations. 3. In reinnervating muscles, spontaneous release was not dependent on Ca2+ entry through either P\u2010 or L\u2010type VDCCs. Neither 100 nM omega\u2010AgaIVA nor 10 microM nitrendipine affected the miniature endplate potential (MEPP) frequency or amplitude. 4. At the newly formed endplates, K(+)\u2010evoked release was dependent on Ca2+ entry through VDCCs of the P\u2010type family (100 nM omega\u2010AgaIVA reduced approximately 70% of the K(+)\u2010evoked MEPP frequency). L\u2010type VDCCs were found not to participate in this type of release (10 microM nitrendipine lacked any effect). 5. In reinnervating muscles, the L\u2010type VDCC blocker, nitrendipine (10 microM), provoked a significant increase (approximately 25%) in the latency of the evoked endplate potential (EPP). This drug also caused an increase (approximately 0.3 ms) in the latency of the presynaptic currents. The P\/Q\u2010 and Ny\u2010type VDCC blockers did not affect the latency of the EPP. 6. These results show that at newly formed mouse neuromuscular junctions, as occurs in mature preparations, VDCCs of the P\u2010type family play a prominent role in evoked transmitter release whereas N\u2010type channels are not involved in this process. In addition, signal conduction and transmitter release become highly sensitive to nitrendipine during reinnervation. This suggests that L\u2010type VDCCs may play a role in synaptic transmission at the immature mammalian neuromuscular junction.<\/jats:p>","DOI":"10.1113\/jphysiol.1996.sp021800","type":"journal-article","created":{"date-parts":[[2014,12,17]],"date-time":"2014-12-17T01:50:46Z","timestamp":1418781046000},"page":"687-697","source":"Crossref","is-referenced-by-count":78,"title":["Calcium channels involved in synaptic transmission at the mature and regenerating mouse neuromuscular junction."],"prefix":"10.1113","volume":"497","author":[{"given":"E","family":"Katz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"P A","family":"Ferro","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"G","family":"Weisz","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"O D","family":"Uchitel","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[1996,12,15]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1996.sp021800","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1996.sp021800","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,27]],"date-time":"2023-10-27T05:48:30Z","timestamp":1698385710000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1996.sp021800"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1996,12,15]]},"references-count":0,"journal-issue":{"issue":"3","published-print":{"date-parts":[[1996,12,15]]}},"alternative-id":["10.1113\/jphysiol.1996.sp021800"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1996.sp021800","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1996,12,15]]}}}