{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,15]],"date-time":"2026-09-15T02:17:49Z","timestamp":1789438669263,"version":"build-2803163510"},"reference-count":69,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2009,2,2]],"date-time":"2009-02-02T00:00:00Z","timestamp":1233532800000},"content-version":"vor","delay-in-days":2377,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[2002,8]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Acetylcholine release at the neuromuscular junction relies on rapid, local and transient calcium increase at presynaptic active zones, triggered by the ion influx through voltage\u2010dependent calcium channels (VDCCs) clustered on the presynaptic membrane. Pharmacological investigation of the role of different VDCC subtypes (L\u2010, N\u2010, P\/Q\u2010 and R\u2010type) in spontaneous and evoked acetylcholine (ACh) release was carried out in adult mouse neuromuscular junctions (NMJs) under normal and pathological conditions.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>\u03c9\u2010Agatoxin IVA (500 n<jats:sc>M<\/jats:sc>), a specific P\/Q\u2010type VDCC blocker, abolished end plate potentials (EPPs) in normal NMJs. However, when neurotransmitter release was potentiated by the presence of the K<jats:sup>+<\/jats:sup> channel blocker 4\u2010aminopyridine (4\u2010AP), an \u03c9\u2010agatoxin IVA\u2010 and \u03c9\u2010conotoxin MVIIC\u2010resistant component was detected. This resistant component was only partially sensitive to 1 \u03bc<jats:sc>M<\/jats:sc> \u03c9\u2010conotoxin GVIA (N\u2010type VDCC blocker), but insensitive to any other known VDCC blockers. Spontaneous release was dependent only on P\/Q\u2010type VDCC in normal NMJs. However, in the presence of 4\u2010AP, it relied on L\u2010type VDCCs too.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>ACh release from normal NMJs was compared with that of NMJs of mice passively injected with IgGs obtained from patients with Lambert\u2010Eaton myasthenic syndrome (LEMS), a disorder characterized by a compromised neurotransmitter release. Differently from normal NMJs, in LEMS IgGs\u2010treated NMJs an \u03c9\u2010agatoxin IVA\u2010resistant EPP component was detected, which was only partially blocked by calciseptine (1 \u03bc<jats:sc>M<\/jats:sc>), a specific L\u2010type VDCC blocker.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>Altogether, these data demonstrate that multiple VDCC subtypes are present at the mouse NMJ and that a resistant component can be identified under \u2018pharmacological\u2019 and\/or \u2018pathological\u2019 conditions.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (2002) <jats:bold>136<\/jats:bold>, 1135\u20131145. doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0704818\">10.1038\/sj.bjp.0704818<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0704818","type":"journal-article","created":{"date-parts":[[2002,9,18]],"date-time":"2002-09-18T00:15:48Z","timestamp":1032308148000},"page":"1135-1145","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":57,"title":["Calcium channel subtypes contributing to acetylcholine release from normal, 4\u2010aminopyridine\u2010treated and myasthenic syndrome auto\u2010antibodies\u2010affected neuromuscular junctions"],"prefix":"10.1111","volume":"136","author":[{"given":"F","family":"Giovannini","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"E","family":"Sher","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"R","family":"Webster","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J","family":"Boot","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"B","family":"Lang","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"311","published-online":{"date-parts":[[2009,2,2]]},"reference":[{"key":"e_1_2_7_2_1","doi-asserted-by":"publisher","DOI":"10.1111\/j.1469-7793.2000.00203.x"},{"key":"e_1_2_7_3_1","doi-asserted-by":"publisher","DOI":"10.1016\/0006-8993(87)90599-3"},{"key":"e_1_2_7_4_1","first-page":"672","article-title":"Dihydropyridine\u2010sensitive and \u2010insensitive components of acetylcholine release from rat motor nerve terminals","volume":"251","author":"ATCHISON W.D.","year":"1989","journal-title":"J. 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