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Alcohol also inhibits the primary excitatory neurotransmitter in the CNS, glutamate. Benzodiazepines also bind to the GABA receptor, making them useful in alcohol withdrawal. This tolerance partly explains the alertness of chronic alcohol users at blood alcohol levels that in others would cause coma or death. With chronic alcohol use, the number of GABA receptors is increased, requiring more and more alcohol to create the same level of inhibition. Alcohol binds strongly to GABA receptors, activating the inhibitory cascade, which results in sedation, cognitive dysfunction, and decreased coordination.

GABA binds to receptors allowing chloride to enter the cell, which decreases cellular excitability.

Gamma-aminobutyric acid (GABA) is the primary CNS inhibitory neurotransmitter. The primary site of action in acute toxicity is the central nervous system, where it increases central nervous system (CNS) inhibition and decreases excitation. It is primarily metabolized in the liver by alcohol dehydrogenase to acetaldehyde. Alcohol is absorbed through the proximal GI tract.

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