EFFECTS OF HYPOTHALAMIC LESIONS ON THE SECRETION AND STORAGE OF HYPOPHYSIAL LUTEINIZING HORMONE

Abstract

Hypothalamic lesions in the median eminence of the tuber cincrcum produced a syndrome of constant vaginal diestrus (CD), accompanied by atrophic ovaries and uteri and a significant decrease in weight of the pars distalis. The ovaries of these rats were characterized by failure of follicular development and the persistence of large corpora lutea. Lesions in the rostral hypothalamus, on the other hand, produced a syndrome of constant vaginal estrus (CE), accompanied by atrophic ovaries, and enlargement of uteri and pars distalis. The ovaries of these rats were filled with large follicles, and there was a scarcity of corpora lutea or their remnants. Using the ovarian ascorbic acid depletion method, LH was measured in plasma and pars distalis before and after ovariectomy in normal rats and those with hypothalamic lesions. No detectable LH was found in plasma from normal rats, but detectable quantities of the hormone were found one to 16-weeks postovariectomy. Hypothalamic lesions producing CD or CE prevented this elevation of plasma LH following ovariectomy. Pituitary LH content was diminished to 33% of normal in rats with CE but was only 15% of normal in rats with CD. Ovariectomy produced a rise in pituitaiy LH content in normal rats and those with CE, whereas this response was blocked in rats with CD. It was concluded that the hypothalamus exerts a regulatory influence over synthesis and secretion of hypophysial LH.