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Effects of Maternal Ethanol Consumption and Buspirone Treatment on Dopamine and Norepinephrine Reuptake Sites and D1 Receptors in Offspring
Author(s) -
Gillespie Roberta A.,
Eriksen Jason,
Hao HongLin,
Druse Mary J.
Publication year - 1997
Publication title -
alcoholism: clinical and experimental research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.267
H-Index - 153
eISSN - 1530-0277
pISSN - 0145-6008
DOI - 10.1111/j.1530-0277.1997.tb03790.x
Subject(s) - buspirone , medicine , offspring , endocrinology , reuptake , dopamine , dorsal raphe nucleus , agonist , serotonergic , serotonin , chemistry , pharmacology , receptor , biology , pregnancy , genetics
Previously, it was shown that in utero ethanol exposure results in decreased serotonin (5‐HT) and altered concentrations of 5‐HT reuptake sites and 5‐HT 1A receptors in fetal and/or postnatal rats. Because fetal 5‐HT is an essential trophic factor, this laboratory previously investigated the hypotheses that the early ethanol‐associated 5‐HT deficit contributed to subsequent development abnormalities in the serotonergic system and that the effects of the fetal 5‐HT deficit could be prevented by maternal treatment with buspirone, a 5‐HT 1A receptor agonist. The present report determined the effects of maternal treatment with buspirone on two other neurotransmitter systems in the developing offspring of ethanol‐fed dams: dopamine (DA) and norepinephrine reuptake sites and D1 receptors in postnatal day 19 offspring of control and ethanol‐fed dams, that received daily injections of saline or 4.5 mg/kg buspirone. These investigations found that in utero ethanol exposure significantly decreased norepinephrine reuptake sites in the dorsomedial hypothalamic nucleus and anteroventral thalamic nucleus. There was also an ethanol effect in the dorsal raphe. D1 receptors were moderately increased (5–10% increase) in the striaturn, and DA reuptake sites were unchanged in PN19 ethanol‐exposed offspring. No other significant ethanol‐related effects were noted. Maternal buspirone treatment did not adversely affect the concentration of DA reuptake sites or D1 receptors in control rats. Thus, whereas buspirone exerts protective effects on the developing 5‐HT system of ethanol‐exposed rats, it does not appear to damage the development of the DA system. Maternal buspirone produced only one significant abnormality in control offspring; it resulted in a significant reduction of norepinephrine reuptake sites in the DR.