CALCIUM-CHANNEL BLOCKERS AND TRANSMITTER RELEASE AT THE NORMAL HUMAN NEUROMUSCULAR-JUNCTION

Transmitter release evoked by nerve stimulation is highly dependent on Ca2+ entry through voltage-activated plasma membrane channels. Calciu m influx may be modified in some neuromuscular diseases like Lambert-E aton syndrome and amyotrophic lateral sclerosis. We studied the pharma cologic sensitivity of the transmitter release process to different ca lcium channel blockers in normal human muscles and found that funnel w eb toxin and omega-Agatoxin-IVA, both P-type calcium channel blockers, blocked nerve-elicited muscle action potentials and inhibited evoked synaptic transmission. The transmitter release was not affected either by nitrendipine, an L-type channel blocker, or omega-Conotoxin-GVIA, an N-type channel blocker. The pharmacologic profile of neuromuscular transmission observed in normal human muscles indicates that P-like ch annels mediate transmitter release at the motor nerve terminals.