Alcohol, alcoholic brain damage, and GABAA receptor isoform gene expression.

Selective variations in cerebral GABAA receptor pharmacology and function are observed in experimental animals subjected to a number of alcohol-treatment and -withdrawal paradigms, and where human alcoholics with and without a range of concomitant diseases are compared with non-alcoholic cases. Recombination studies have shown that variations in GABAA receptor pharmacology and function can result from altering its subunit isoform composition. This commentary examines the rôle of subunit isoform expression in the response to long-term alcohol administration in animals, and in the pathogenesis of alcoholism-related brain damage in human cases.