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Endocrinology, Vol 99, 713-719, Copyright © 1976 by Endocrine Society
ARTICLES |
ME Freeman, FT LaRochelle Jr and RB Moore
This study was designed to describe the effects of thyroid status on the preovulatory surge of LH and to determine the site(s) at which these effects are exerted. The treatment of normal 4-day cycling rats with a hyperthyroid dose of thyroxine (T4, 20 mug/100 g BW/day) for 8 days resulted in surges of LH on proestrus which were depressed to 25% of control levels. In ovariectomized (OV) or ovariectomized- thyroidectomized (OV-Tx) rats maintained on a physiological regimen of T4 (2 mug/100 gBW/day), the amount of estrogen required to induce an LH surge was far greater than that required in OV-TX rats receiving no T4 replacement. These data suggest that T4 attenuates preovulatory surges of LH by acting at the hypothalamic-pituitary axis. However, the pituitary might be eliminated as a site of action since hyerthyroid proestrous rats responded to a challenge of LH-releasing hormone (500 ng) by secreting a quantity of LH equivalent to that in euthyroid animals. Similarly, there was no difference in the quantity of LH released by hyperthyroid and euthyroid proestrous rats in response to electrochemical stimulation (100 muA, 60 sec) of the medial preoptic area of the hypothalamus. On the other hand, hyperthyroid rats secreted significantly less LH in response to stimulation of the arcuate nucleus- median eminence area (ARN-ME) than did controls. Thus, T4, apparently modifies LH release by depressing the response of the ARN.
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N. Vasudevan, S. Ogawa, and D. Pfaff Estrogen and Thyroid Hormone Receptor Interactions: Physiological Flexibility by Molecular Specificity Physiol Rev, October 1, 2002; 82(4): 923 - 944. [Abstract] [Full Text] [PDF] |
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