Dendrotoxin, 4‐Aminopyridine, and β‐Bungarotoxin Act at Common Loci but by Two Distinct Mechanisms to Induce Ca2+‐Dependent Release of Glutamate from Guinea‐Pig Cerebrocortical Synaptosomes
- 1 January 1989
- journal article
- research article
- Published by Wiley in Journal of Neurochemistry
- Vol. 52 (1), 201-206
- https://doi.org/10.1111/j.1471-4159.1989.tb10917.x
Abstract
The release of endogenous glutamate from guinea pig cerebrocortical synaptosomes evoked by dendrotoxin, .beta.-bungarotoxin, and 4-aminopyridine is compared. Dendrotoxin and 4-aminopyridine cause Ca2+-dependent release, representing a partial depletion of the KCl-releasable transmitter pool. The decrease in the plasma membrane potential caused by 4-aminopyridine or dendrotoxin and the evoked release of glutamate from a transmitter pool accord with the inhibitory action of these agents on certain K+ conductances. In contrast, the massive release of glutamate evoked by .beta.-bungarotoxin is produced in the presence of Ca2+ but not of Sr2+, a result consistent with a generalised permeabilisation of synaptosomal plasma membranes. Although dendrotoxin inhibits the binding of .beta.-bungarotoxin and the resultant synaptosomal lysis, demonstration of a direct effect of .beta.-bungarotoxin binding per se on K+ permeability is impractical owing to its phospholipase A2 activity.Keywords
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