A hypothalamic luteinizing-hormone-releasing factor

¹ Department of Physiology, School of Medicine, University of Pennsylvania, Philadelphia, Pennsylvania

Crude acidic extracts of rat stalk-median eminence tissue evoked an ovarian ascorbic acid depletion on intravenous injection into immature rats pretreated with gonadotropins. Response was linearly related to logarithm of the dose. Various parts of the hypothalamus were extracted, and the major activity was found to reside in the stalk-median eminence region. Activity of this stalk-median eminence extract (SME) was relatively heat stable as compared to luteinizing hormone (LH) activity of rat anterior pituitary extract. SME was partially inactivated by pepsin and completely inactivated by tryptic digestion. Intravenous SME did not elevate the already high plasma LH levels in untreated ovariectomized rats but evoked a significant elevation in plasma LH of ovariectomized, estrogenized donors, whereas an extract of cerebral cortex was ineffective in this latter type of test animal. Pitressin also failed to influence LH titer of such donors. Increasing doses of estrogen or estrogen plus progesterone failed to block this effect of SME. SME also increased LH activity in plasma of ovariectomized rats in which release of LH had been blocked by lesions in the median eminence. It elevated LH activity in plasma of normal donors but had no significant effect on plasma LH activity of hypophysectomized animals. It was concluded that a hypophysial LH-releasing factor resides in stalk-median eminence tissue, and reasons were advanced for believing this to be a hormonal effect.