Prenatal Ethanol Exposure Impairs Dopamine D2 and Serotonin Agonist Effects in Rats

Document Type

Article

Publication Date

12-1-1996

Description

Prolonged prenatal exposure to ethanol produces long-lasting alterations in the level of endogenous brain biogenic amines in rats. To test whether there might be long-lived alterations in the reactivity to dopaminergic, serotoninergic or muscarinic agonists in rats exposed prenatally to ethanol, the following study was done. Wistar rats were given 10% (v/v) ethanol in drinking water, starting 10 days before mating and continuing to the end of pregnancy. Male offspring were tested at 3 months for characteristic behavioral effects (oral activity) known to be induced by agonists acting at central dopamine D2 (quinpirole), serotonin 5-HT2C (m-chlorophenylpiperazine, m-CPP) and muscarine (pilocarpine) receptors. Dose-effect curves demonstrated that oral activity responses to quinpirole HCl (0.05-0.40 mg/kg i.p.) and m-CPP 2HCl (0.3-6.0 mg/kg i.p.) were greatly reduced (P < .001) in rats that were exposed to ethanol in utero. Responses to pilocarpine HCl (0.1-3.0 mg/kg) remained unaltered. The findings indicate that prenatal ethanol exposure alters behavioral responses to D2 and 5-HT2C agonists in male rats tested three months after birth. We propose that prenatal ethanol diminishes reactivity of receptors for dopamine D2 and serotonin 5-HT2C receptors.

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