Presynaptic Inhibition in Cuneate blocked by GABA Antagonists

BICUCULLINE has been shown to have an action essentially similar to Picrotoxin in antagonizing both synaptically evoked postsynaptic inhibition and the depressant action of γ-amino-butyric acid (GABA) on cuneate neurones¹. This supports the hypothesis that GABA is the postsynaptic inhibitory transmitter in the cuneate². However, evidence³ indicates that GABA has a dual action in the cuneate, not only depressing the excitability of postsynaptic neurones, but also increasing the excitability of primary afferent terminals in a manner which might be expected of a presynaptic inhibitory transmitter. The experiments reported here show that the alkaloids bicuculline and picrotoxin block presynaptic inhibition and that this action is consistent with them exerting a GABA-antagonist action at primary afferent terminals.