Pflügers Archiv

, Volume 434, Issue 6, pp 735–741

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

  • W. Van der Kloot
  • Jordi Molgó
  • Ligia A. Naves
ORIGINAL ARTICLE

DOI: 10.1007/s004240050459

Cite this article as:
Van der Kloot, W., Molgó, J. & Naves, L. Pflügers Arch (1997) 434: 735. doi:10.1007/s004240050459

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, 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.

Key words AcetylcholineQuantal releaseAutoinhibitionFacilitationω-ConotoxinsSynapseCarbachol

Copyright information

© Springer-Verlag Berlin Heidelberg 1997

Authors and Affiliations

  • W. Van der Kloot
    • 1
  • Jordi Molgó
    • 2
  • Ligia A. Naves
    • 3
  1. 1.Department of Physiology and Biophysics, SUNY at Stony Brook, Stony Brook, NY 11794-8661,USAUS
  2. 2.Laboratoire de Neurobiologie Cellulaire et Moléculaire, CNRS, F-91198 Gif sur Yvette, Cedex, FranceFR
  3. 3.Dept. of Physiology and Biophysics, Federal University of Minas Gerais, Belo Horizonte, MG, BrazilBR