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 microM) though, the Ca2+ current duration decreased from greater than 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 microM) and pirenzepine (3 microM), 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.
Hamilton
B R
BR
Department of Physiology, University of Wisconsin, Madison 53706.
Smith
D O
DO
D000109:Acetylcholine / Q000502:physiology; D000200:Action Potentials / Q000502:physiology; D000255:Adenosine Triphosphate / Q000502:physiology; D000818:Animals; D002118:Calcium / Q000502:physiology; D002121:Calcium Channel Blockers / Q000494:pharmacology; D015220:Calcium Channels / Q000378:metabolism*; D004558:Electric Stimulation; D004594:Electrophysiology; D005246:Feedback; D009046:Motor Neurons / Q000378:metabolism*; D009132:Muscles / Q000294:innervation; D009411:Nerve Endings / Q000378:metabolism*; D015221:Potassium Channels / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D011950:Receptors, Cholinergic / Q000502:physiology; D013779:Tetrodotoxin / Q000494:pharmacology
D002121:Calcium Channel Blockers; D015220:Calcium Channels; D015221:Potassium Channels; D011950:Receptors, Cholinergic; D013779:Tetrodotoxin; D000255:Adenosine Triphosphate; D000109:Acetylcholine; D002118:Calcium