Abstract
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.
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DAVIDSON, N., REISINE, H. Presynaptic Inhibition in Cuneate blocked by GABA Antagonists. Nature New Biology 234, 223–224 (1971). https://doi.org/10.1038/newbio234223a0
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DOI: https://doi.org/10.1038/newbio234223a0
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