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PubMed · 9306006

Cholinergic agonists decrease quantal output at the frog neuromuscular junction by targeting a calcium channel blocked by omega-conotoxin.

W Van der Kloot·J Molgó·L A Naves
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Abstract

Nicotinic cholinergic agonists are known to decrease synchronous evoked quantal output at the frog neuromuscular junction [Van der Kloot 1993, J Physiol (Lond) 468:567-589]. Here we also show that carbachol decreases the frequency of miniature endplate potentials (FMEPP) in solutions containing elevated levels of K+ and Ca2+. Carbachol did not decrease FMEPP in hypertonic solutions or in solutions containing the Ca2+ ionophore ionomycin and Ca2+. We conclude that the nicotinic agonists decrease Ca2+ influx through voltage-gated Ca2+ channels. Carbachol did not alter two-pulse facilitation. A blocker of N-type Ca2+ channels, omega-conotoxin GVIA, antagonized the nicotinic agonist-induced decrease in evoked quantal output. The effect of carbachol was not altered by omega-conotoxin MVIIC, a blocker of P-type and certain other Ca2+channels. The Ca2+ channel targeted by the nicotinic agonists appears to be of the N-type.

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AnimalsCalcium Channel BlockersCalcium ChannelsCholinergic AgentsElectrophysiologyHypertonic SolutionsIonomycinIonophoresMotor EndplateNeuromuscular JunctionPeptidesPotassiumRana pipiensSolutionsomega-Conotoxin GVIAomega-ConotoxinsJournal ArticleResearch Support, Non-U.S. Gov'tResearch Support, U.S. Gov't, P.H.S.

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W Van der Kloot, J Molgó, L A Naves. 1997. Cholinergic agonists decrease quantal output at the frog neuromuscular junction by targeting a calcium channel blocked by omega-conotoxin.. https://doi.org/10.1007/s004240050459

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