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

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Abstract
The release of endogenous glutamate from guineapig cerebrocortical synaptosomes evoked by dendrotoxin, β‐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 β‐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 β‐bungarotoxin and the resultant synaptosomal lysis, demonstration of a direct effect of β‐bungarotoxin binding per se on K+ permeability is impractical owing to its phospholipase A2 activity.

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