Abstract
The effect of chronic ethanol administration on [ 3H]zolpidem binding was measured in rat brain. [ 3H]Zolpidem selectively labels γ-aminobutyric acid A-benzodiazepine type 1 receptors, which are highly correlated with ethanol-sensitive γ-aminobutyric acid (GABA) responses in brain. Recombinant expression studies have suggested that this GABA A receptor subtype requires the expression of α 1 subunits and is not selectively labeled by classic GABAergic ligands. Since chronic ethanol administration reduces α 1 subunit mRNA and polypeptide levels, we investigated whether alterations in [ 3H]zolpidem binding would also be detected. Chronic ethanol administration did not reduce [ 3H]zolpidem binding. Instead small, but reproducible, increases in [ 3H]zolpidem binding density were detected in cortex and cerebellum with no change in affinity. No alterations in [ 3H]zolpidem binding to striatum and hippocampus were observed. Thse findings suggest that chronic ethanol administration may have differential effects on [ 3H]zolpidem binding sites and α 1 subunit expression. Alterations in α 1 subunit expression following chronic ethanol administration may involve other GABA A receptor subtypes or high affinity [ 3H]zolpidem binding may be dependent on the expression of additional GABA A receptor units.
Published Version
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