Abstract
In the human central nervous system, the gamma-aminobutyric acid (GABA) type A receptor complex undergoes changes with both acute and chronic exposure to sedative-hypnotic drugs. These changes contribute to both the acute effects of these drugs as well as the chronic effects of sedative-hypnotic dependence, withdrawal, and drug craving. Clinically these chronic effects are difficult to treat in patients dependent on ethanol or benzodiazepines. Valproate may return the GABA type A receptor function to a state more closely resembling its normal function. By this mechanism, it is possible to reduce the symptoms of sedative-hypnotic withdrawal and relapse.
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