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Prenatal Ethanol Exposure Selectively Reduces the mRNA Encoding α‐1 Thyroid Hormone Receptor in Fetal Rat Brain
Author(s) -
Scott Heather C.,
Sun Grace Y.,
Zoeller R. Thomas
Publication year - 1998
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.1530-0277.1998.tb05924.x
Subject(s) - neocortex , endocrinology , medicine , thyroid , hormone , fetus , hippocampus , fetal alcohol syndrome , thyroid hormone receptor , receptor , biology , ethanol , pregnancy , neuroscience , biochemistry , genetics
Some of the developmental defects characteristic of congenital or experimental hypothyroidism are also observed in children or experimental animals prenatally exposed to ethanol, suggesting that a subset of neurological defects attributable to ethanol exposure are produced by interfering with thyroid hormone action. In this article, we tested whether an ethanol treatment regimen known to produce neurological damage in rats can alter the expression of the mRNAs encoding the thyroid hormone receptor isoforms (TR α‐1, TR α‐2, and TR α‐1) in the fetal rat brain neocortex and hippocampus. Rats were fed an ethanol‐containing diet beginning on gestational day (G) 6 and continuing until sacrifice on G15, G17, or G21; controls included animals pair‐fed a liquid control diet or fed lab chow. Ethanol selectively reduced the expression of TR a‐1 mRNA in the neocortex and hippocampus on G21, compared with pair‐fed and control fetuses. In contrast, pair‐feeding selectively reduced TR a‐2 mRNA in both neocortex and hippocampus on G21, and increased TR 0–1 mRNA on G17. These data support the hypothesis that ethanol may interfere with thyroid hormone action during fetal brain development In addition, these data indicate that ethanol and pair‐feeding exert independent effects on thyroid hormone receptor expression in the developing brain.