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Nature of the postsynaptic action of crotoxin at guinea-pig diaphragm end-plates

O V Brazil1, M D Fontana, N F Heluany

  • 1Department of Pharmacology, Faculty of Medical Sciences, State University of Campinas (UNICAMP), SP, Brazil.

Journal of Natural Toxins
|March 4, 2000
PubMed

Insights

Crotoxin causes blockade at mammalian muscle end-plates by desensitizing nicotinic receptors. This effect is reversed by 4-aminopyridine (4-AP), confirming a receptor desensitization mechanism, not a curaremimetic action.

Area of Science:

  • Neuroscience
  • Pharmacology
  • Toxicology

Background:

  • Crotoxin is a neurotoxin known to affect nicotinic receptors in non-mammalian species.
  • The mechanism of crotoxin's action at mammalian neuromuscular junctions remains unclear.

Purpose of the Study:

  • To determine if crotoxin's postsynaptic effect at mammalian muscle end-plates is due to receptor desensitization or a curaremimetic action.
  • To investigate the role of 4-aminopyridine (4-AP) in modulating crotoxin's effects.

Main Methods:

  • Experiments were conducted on guinea-pig diaphragms.
  • Miniature end-plate potentials (m.e.p.p.s) and carbachol-induced end-plate depolarization were measured.
  • The effects of crotoxin, 4-aminopyridine (4-AP), neostigmine, d-tubocurarine (dTc), and beta-bungarotoxin (beta-BTX) were assessed.

Main Results:

  • Crotoxin blocked m.e.p.p.s at low concentrations, an effect antagonized by 4-AP.
  • 4-AP did not restore m.e.p.p.s blocked by dTc or beta-BTX.
  • Crotoxin-induced blockade of carbachol-evoked depolarization was also antagonized by 4-AP.

Conclusions:

  • The postsynaptic effect of crotoxin at the guinea-pig muscle end-plate is caused by nicotinic receptor desensitization.
  • 4-aminopyridine (4-AP) acts as an antagonist to this crotoxin-induced receptor desensitization.

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