Perinatal thiouracil exposure depresses corticotropin-releasing factor activity in 15 day old rats.

Medical University of Ohio at Toledo, Toledo, Ohio, United States
Hormone and Metabolic Research (Impact Factor: 2.04). 11/1983; 15(10):488-90. DOI: 10.1055/s-2007-1018766
Source: PubMed

ABSTRACT Although previous in vivo studies have shown thiouracil to delay maturation of the hypothalamus-pituitary-adrenal (HPA) axis response to stress, the nature of the developmental deficit was not determined. By in vitro methods we determined which HPA components are influenced by thiouracil-induced hypothyroidism in 15 day old rats. Our results indicate that adrenal response to ACTH stimulation and adenohypophysial ACTH content were not significantly modified by thiouracil exposure. On the other hand, the corticotropin-releasing factor-like activity of median eminence extracts was severely depressed by thiouracil-induced hypothyroidism. Thus, the delayed maturation of functional capacity of the central nervous system caused by hypothyroidism includes synthesis of biologically active corticotropin-releasing factor.

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    ABSTRACT: Depression of thyroid status with thiouracil has been shown to delay the response of the hypothalamus-pituitary-adrenal axis to stress in young rats. In vivo and in vitro bioassay studies have indicated that the hypothalamus is the main site of axis alteration in 15 day old animals. The present study has found a significantly depressed hypothalamic content of immunoassayable corticotropin-releasing factor (CRF) in thiouracil treated young rats.
    Hormone and Metabolic Research 01/1985; 16(12):674-5. DOI:10.1055/s-2007-1014881 · 2.04 Impact Factor
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    ABSTRACT: The role of thyroid hormones on the development of intracellular glucocorticoid receptor concentrations was examined in the hippocampus, hypothalamus, and pituitary of the rat. Adult animals, administered triiodothyronine (T3; 1.0 micrograms/g body weight) on days 1, 2, and 4 of life or thyroxine (T4; 2.5 micrograms/g body weight) on days 1 and 2 of life, had significantly elevated glucocorticoid receptor concentrations in the hippocampus, but not in hypothalamus or pituitary. Adult animals treated with propylthiouracil (PTU; 0.2% in the mother's food), a thyroid hormone synthesis inhibitor, for the first 2 weeks of life showed decreased glucocorticoid receptor concentrations in hippocampus, but not in hypothalamus or pituitary. We then examined whether thyroid hormones might mediate the effects of early stimulation on the development of hippocampal glucocorticoid receptor concentrations. Animals that were handled for 15 min daily (Ha) for the first 2 weeks of life showed increased hippocampal glucocorticoid receptor concentrations as adults compared to nonhandled (NHa) controls. PTU administration blocked the effects of handling, such that Ha/PTU animals showed hippocampal glucocorticoid receptor concentrations that were indistinguishable from those of NHa animals. In contrast, corticosterone administration over the first 2 weeks of life had no effect on adult hippocampal glucocorticoid receptor concentrations. These data suggest that thyroid hormones mediate, in part at least, the development of glucocorticoid receptor concentrations in the hippocampus and that this effect occurs independently of their effects on corticosterone titers.
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