Omega-conotoxin does not block the verapamil-sensitive calcium channels at mouse motor nerve terminals

Abstract

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.