Omega-conotoxin does not block the verapamil-sensitive calcium channels at mouse motor nerve terminals.
Release of acetylcholine at the neuromuscular junctions of skeletal muscle is not sensitive to organic Ca2+ channel blockers. However, in mouse motor nerve endings, extracellular recording reveals that a verapamil-sensitive Ca2+ current can be induced after block of K+ channels. Recordings of extracellular action potentials from inside the perineural sheaths of nerves innervating mouse triangularis sterni muscles reveal that this verapamil-sensitive current is not blocked by omega-conotoxin, and hence, it does not involve channels similar to the L-channels of neuronal cell bodies.
D000818:Animals; D001001:Anura; D002118:Calcium / Q000378:metabolism*; D007473:Ion Channels / Q000187:drug effects*; D008297:Male; D051379:Mice; D008807:Mice, Inbred BALB C; D008978:Mollusk Venoms / Q000494:pharmacology*; D009407:Nerve Block; D009469:Neuromuscular Junction / Q000378:metabolism*; D014700:Verapamil / Q000494:pharmacology*; D020960:omega-Conotoxins
D007473:Ion Channels; D008978:Mollusk Venoms; D020960:omega-Conotoxins; C053423:Conus magus toxin; D014700:Verapamil; D002118:Calcium