Abstract
Considerable progress has been made in our understanding of the cellular mechanisms of action of alcohol on the brain, particularly in relation to tolerance and dependence. Tolerance is associated with changes in the composition of the gamma-aminobutyric acid-benzodiazepine receptor, making it less sensitive to alcohol. An increased density of excitatory glutamate receptors may underlie certain withdrawal manifestations. Other neuroadaptive mechanisms include an increase in presynaptic calcium influx on depolarization and effects on adenylate cyclase. Alcohol also influences the expression of a proto-oncogene which plays an important role in neural development. Further advances in neurobiology offer the prospect of elucidating the mechanisms of tolerance and brain damage.
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