Cholinergic agonists decrease quantal output at the frog neuromuscular junction by targeting a calcium channel blocked by ω-conotoxin |
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Authors: | W Van der Kloot Jordi Molgó Ligia A Naves |
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Institution: | (1) Department of Physiology and Biophysics, SUNY at Stony Brook, Stony Brook, NY 11794-8661,USA, US;(2) Laboratoire de Neurobiologie Cellulaire et Moléculaire, CNRS, F-91198 Gif sur Yvette, Cedex, France, FR;(3) Dept. of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, MG, Brazil, BR |
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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 (F
MEPP) in solutions containing elevated levels of K+ and Ca2+. Carbachol did not decrease F
MEPP 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, ω-conotoxin GVIA, antagonized the nicotinic agonist-induced decrease in evoked quantal output. The effect of carbachol
was not altered by ω-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.
Received: 6 March 1997 / Received after revision: 6 May 1997 / Accepted: 4 June 1997 |
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Keywords: | Acetylcholine Quantal release Autoinhibition Facilitation ω -Conotoxins Synapse Carbachol |
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