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Cholinergic agonists decrease quantal output at the frog neuromuscular junction by targeting a calcium channel

W Van der Kloot1, J Molgó, L A Naves

  • 1Department of Physiology and Biophysics, SUNY at Stony Brook, Stony Brook, NY 11794-8661,USA.

Pflugers Archiv : European Journal of Physiology
|November 5, 1997
PubMed
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Nicotinic agonists, like carbachol, reduce neurotransmitter release at the frog neuromuscular junction by decreasing calcium (Ca2+) influx through N-type voltage-gated calcium channels.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Cellular Physiology

Background:

  • Nicotinic cholinergic agonists are known to reduce neurotransmitter release at the frog neuromuscular junction.
  • The precise mechanism by which these agonists affect quantal output, particularly miniature endplate potentials, requires further elucidation.

Purpose of the Study:

  • To investigate the effect of carbachol on miniature endplate potentials (FMEPP) in frog neuromuscular preparations.
  • To determine the role of calcium (Ca2+) influx and specific calcium channel subtypes in mediating the actions of nicotinic agonists.

Main Methods:

  • Measurements of evoked quantal output and miniature endplate potentials (FMEPP) in frog neuromuscular junctions.
  • Application of carbachol in solutions with varying K+ and Ca2+ concentrations, hypertonic solutions, and in the presence of Ca2+ ionophores.

Related Experiment Videos

  • Utilized specific calcium channel blockers: omega-conotoxin GVIA (N-type) and omega-conotoxin MVIIC (P-type and others).

    • Main Results:

    • Carbachol decreased FMEPP in solutions with elevated K+ and Ca2+, but not in hypertonic solutions or with ionomycin.
    • Carbachol did not affect two-pulse facilitation.
    • Omega-conotoxin GVIA, an N-type Ca2+ channel blocker, antagonized the carbachol-induced decrease in evoked quantal output.
    • Omega-conotoxin MVIIC did not alter the effect of carbachol.

    Conclusions:

    • Nicotinic agonists decrease Ca2+ influx through voltage-gated Ca2+ channels.
    • The targeted Ca2+ channels are predominantly of the N-type.
    • This action contributes to the reduction in neurotransmitter release observed with nicotinic agonists.