We have recently reported immunoassayable luteinizing hormone (LH) in several areas of the rat brain and conspicuously present in the hypothalamus. In this report, we focus on the presence of LH in the hypothalamus and its potential role in regulation of pituitary LH release. In adult female rats, examined during the course of the estrous cycle, a significant fall in hypothalamic LH coincides with the surge in pituitary and serum LH at the time of proestrus, signaling ovulation. Ovariectomized adult rats show no change in hypothalamic LH at a time when there is a dramatic rise in both anterior pituitary and serum LH. These data support the concept that hypothalamic LH is not of pituitary origin and that it may play a role in the short-loop negative feedback system controlling the surge in anterior pituitary LH release, an event initiating ovulation.
A simplified fluorometric procedure for corticosterone or hydrocortisone has been described. In spite of certain specificity limitations, it has practical applications for the estimation of these steroids in samples that are small in volume or low in concentration, or in studies that are designed primarily to demonstrate increases or decreases in adrenocortical hormones in plasma or adrenals without requiring absolute specificity. For rat, human, monkey, or guinea pig plasma, 0.5 ml. suffices for an analysis. One rat adrenal or a fraction of a guinea pig adrenal usually contains enough steroid for a single determination.
A procedure also has been described which can be applied to rat plasma to correct for interfering fluorescent material.
The coexistence of hyperparathyroidism and thyroid tumors and/or chronic thyroiditis has raised the possibility of an etiologic relationship. The present study was designed to test the hypothesis that the chronic elevation of thyroid-stimulating hormone (TSH) is related to the development of hyperparathyroidism. Three groups of 24 rats each were treated for 12 weeks as follows: group 1 received propylthiouracil (PTU) in their deionized water; group 2 received PTU and thyroid hormone to suppress TSH and to serve as a control group for possible direct effects of PTU; and group 3 was not treated at all and served as another control group. At 12 weeks, 95% of group 1 rats (PTU only) showed hyperplasia of the parathyroids with a 30% mean increase in circulating parathormone.
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