{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,7]],"date-time":"2026-10-07T03:16:37Z","timestamp":1791342997539,"version":"4.3.1"},"reference-count":37,"publisher":"American Physiological Society","issue":"4","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Journal of Neurophysiology"],"published-print":{"date-parts":[[2006,4]]},"abstract":"<jats:p>\n                    Tottering ( Tg) mice carry the mutation P601L in their Cacna1a encoded Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.1 channels. Transmitter release at the wild-type neuromuscular junction (NMJ) is almost exclusively mediated by Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.1 channels, and we used this model synapse to study synaptic consequences of the Tg mutation. With electrophysiology, and using subtype-specific Ca\n                    <jats:sub>v<\/jats:sub>\n                    2 channel-blocking toxins, we assessed a possible compensatory contribution of non-Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.1 channels to evoked acetylcholine (ACh) release at Tg NMJs. Release was reduced by \u223c75% by the Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.1 channel blocker \u03c9-agatoxin-IVA, which was less than the \u223c95% reduction observed in wild-type. Release at Tg NMJs, but not at wild-type synapses, was reduced by \u223c15% by SNX-482, a Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.3 channel blocker. No Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.2 channel involvement was found. Probably, there is a small reduction in functional presynaptic Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.1 channels at Tg NMJs, which is compensated for by Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.3 channels. The remaining Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.1 channels are likely to convey enlarged Ca\n                    <jats:sup>2+<\/jats:sup>\n                    flux, because evoked ACh release at Tg NMJs, at low extracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    concentration, was approximately sixfold higher than at wild-type NMJs. This is the first report of compensatory expression of non-Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.1 channels at NMJs of mice with a single amino acid change in Ca\n                    <jats:sub>v<\/jats:sub>\n                    2.1.\n                  <\/jats:p>","DOI":"10.1152\/jn.01221.2005","type":"journal-article","created":{"date-parts":[[2005,12,28]],"date-time":"2005-12-28T20:13:43Z","timestamp":1135800823000},"page":"2698-2704","source":"Crossref","is-referenced-by-count":27,"title":["Compensatory Contribution of Ca\n                    <sub>v<\/sub>\n                    2.3 Channels to Acetylcholine Release at the Neuromuscular Junction of\n                    <i>Tottering<\/i>\n                    Mice"],"prefix":"10.1152","volume":"95","author":[{"given":"Simon","family":"Kaja","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rob C. 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