Abstract
The effects of chronic ethanol administration and ethanol withdrawal on the kinetic and pharmacological properties of [3H]SCH23390 binding sites and the labelling of central dopamine D-1 receptors were studied in the striatum of the rat. Chronic 40 day ethanol treatment produced a statistically significant decrease (p < 0.05) in maximum binding (Bmax) on striatal dopamine D-1 receptors of the rat, KD remaining unaltered. The withdrawal of ethanol did not affect the kinetic binding parameters. The rank order of potency in displacing the specific [3H]SCH23390 binding of several dopamine antagonists, agonists and serotonin-related drugs was consistent with the pharmacological profile of dopamine D-1 receptors. Chronic ethanol treatment led to a statistically significant increase in receptor affinity (lower Ki than controls) for (+)-butaclamol (p < 0.05). Ethanol withdrawal for 24 hr increased the affinity of [3H]SCH233390-labeled binding sites for norepinephrine. The addition of 0.03–0.68 M ethanol in vitro had no significant effects on [3H]SCH23390 binding in striatal preparations taken from both control and ethanol-treated rats.The results show that rat striatal [3H]SCH23390-labelled binding sites are affected by different conditions of ethanol exposure, possibly suggesting the mediation of striatal dopamine pathways in the responses to ethanol intoxication. © 1997 Elsevier Science Ltd. All rights reserved.
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