The perfused in vitro amphibian spinal cord preparation was used as an experimental model to investigate the effects of alcohol (ethanol) on a complex neural system. Addition of alcohol (150 to 450 mg/100 ml) to the perfusate consistently enhanced primary afferent depolarization (PAD). This was manifested by increased dorsal root (DR) potentials and increased excitability of DR terminals in response to dorsal or ventral root stimulation. As a result of the increased PAD, presynaptic inhibition of orthodromic reflex activity was augmented. It is probable that alcohol brings about these effects by potentiating the action of γ-aminobutyric acid (GABA), the putative transmitter responsible for presynaptic inhibition, since the depolarization of primary afferent terminals elicited by this amino acid was significantly increased following exposure to alcohol.
Davidoff RA. Alcohol and Presynaptic Inhibition in an Isolated Spinal Cord Preparation. Arch Neurol. 1973;28(1):60–63. doi:10.1001/archneur.1973.00490190078011
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