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Alterations in Regional Catecholamine Content and Turnover in the Male Rat Brain in Response to in Utero Ethanol Exposure
Author(s) -
Dewey Cooper J.,
Kevin Rudeen P.
Publication year - 1988
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.1530-0277.1988.tb00195.x
Subject(s) - catecholamine , endocrinology , medicine , in utero , liquid diet , offspring , hypothalamus , dopaminergic , ethanol , midbrain , cerebellum , diencephalon , turnover , basal (medicine) , dopamine , chemistry , central nervous system , biology , pregnancy , fetus , biochemistry , genetics , management , economics , insulin
Fetal ethanol exposure is known to produce CNS abnormalities. The molecular basis for these manifestations observed in animals exposed to ethanol in utero may be explained by changes in regional catecholamine content and turnover. This study was designed to determine changes in catecholamine content and turnover in the cerebral cortex, cerebellum, medial basal hypothalamus, diencephalon, and septal area of male rats exposed to ethanol pre‐ and postnatally. Pregnant Sprague‐Dawley rats were exposed to either an ad libitum liquid diet containing 35% ethanol‐derived calories, an isocalorically matched liquid diet, or a diet consisting of laboratory chow and water. Regional alterations in catecholamine content and turnover in each of the brain areas were observed on postnatal Day 18. A regional variability was demonstrated in the effect of in utero ethanol exposure on catecholamine content and turnover. The most dramatic effect was found in the dopaminergic neurons of the medial basal hypothalamus where in utero ethanol exposed offspring had a significantly reduced DA content and turnover when compared to pups from both isocalorically matched and chow‐fed dams. These data indicate that the dopaminergic neurons of this particular brain region are susceptible to alteration by ethanol exposure during development and that this alteration cannot be explained by changes in nutrition alone.