CALCIUM CURRENTS IN RAT MOTOR-NERVE TERMINALS

Ca2+ currents in response to an action potential were recorded extracellularly under non-voltage clamped conditions from rat motor nerve terminals. The Ca2+ current was blocked by Cd2+, Co2+, and Ni2+. A residual component that could not be blocked by inorganic cations was inhibited completely by tetrodotoxin (TTX). The Ca2+ current was also moderately sensitive to the N- and L-type Ca2+ channel-blocker omega-conotoxin but was insensitive to the L-type channel-specific dihydropyridines. When a fraction of the terminal K+ currents was blocked by 10 mM tetraethylammonium (TEA), the Ca2+ current duration decreased only slightly as stimulation frequency increased from 0.5 to 20 Hz. When K+ currents were blocked by TEA plus 3,4-diaminopyridine (250-mu-M) though, the Ca2+ current duration decreased from > 70 ms to 8-10 ms as stimulation frequency increased from 0.5 to 20 Hz. Recovery of the duration following 20-Hz stimulation occurred faster during subsequent stimulation at 0.5 Hz than at 2 Hz. ATP and ACh inhibit Ca2+ currents at stimulation frequencies ranging from 0.5 to 20 Hz; however, when the purinergic and cholinergic autoreceptors are blocked by theophylline (100-mu-M) and pirenzipine (3-mu-M), respectively, the frequency-induced decrease in current duration persisted. Thus, motor nerve terminal Ca2+ current duration is determined by stimulus repetition frequency; this appears to involve intracellular Ca2+ accumulation, although effects secondary to variability in the time course of changes in terminal membrane potentials cannot be ruled out.