Abstract
γ-Aminobutyric acid (GABA) applied to neurones in the olfactory cortex slice in vitro, increases input conductance and produces a small depolarization, which mimicks the action of the inhibitory transmitter. In previous experiments it was shown that this inhibition could be blocked by picrotoxin, bicuculline, strychnine, leptazol, bemegride, theophylline and d-tubocurarine. In the present study the effects of the above blockers on the action of bathapplied GABA were assessed. These blockers all antagonised the action of GABA at concentrations similar to those required to block synaptic inhibition. However, the amount of antagonism of GABA action was variable and this variability was attributed to the cellular uptake of GABA. The variability was circumvented by using muscimol, a GABA agonist not subjected to uptake. This GABA antagonism explains the convulsant action of many of the agents studied and reinforces the idea that GABA mediated inhibitory transmission in the olfactory cortex.