Altered gonadotropin and prolactin release induced by median eminence (ME) lesions and pharmacological manipulation of prolactin release: Further evidence for separate hypothalamic control of FSH and LH release

Abstract

To delineate more clearly the regions of the median eminence involved in the control of gonadotropin secretion, electrolytic lesions were made in the median eminence of adult male rats. Also the role of prolactin in the maintenance of gonadotropin secretion and sex organs was further evaluated by the administration of α-bromo-ergocryptine (CB154) or its diluent SC to lower prolactin via its dopamine agonist action in these animals with lesions. The effects of elevation of prolactin by the administration in the drinking water of the dopamine antagonist, sulpiride, were also evaluated in intact rats. At the conclusion of the experiments the localization of lesions was carefully evaluated by microscopic examination of serial sections through the hypothalamic region. The results indicate that lesions which completely destroyed the median eminence led to elevation in plasma prolactin and profound decreases in plasma FSH and LH associated with atrophy of testes and accessory sex organs. This result was not affected if CB 154 was given to lower the elevated prolactin levels. Lesions which destroyed the rostral 2/3 of the median eminence were frequently associated with declines in plasma LH and relatively normal plasma FSH, whereas lesions which extended caudally to destroy the posterior median eminence were associated uniformly with a profound lowering of FSH. If these lesions did not include the anterior portions of the median eminence, LH levels remained normal. The results support the concept of separate control of FSH and LH release. LH release appears to be controlled particularly by the rostral 2 3 of the median eminence which is the presumed site of termination of the terminals of LHRH-secreting neurons, whereas FSH release is predominantly controlled by the posterior 2 3 of the median eminence, the presumed termination of the axons of the putative FSH-releasing factor neurons. The development of testicular atrophy and target gland atrophy was more closely associated with low plasma and pituitary FSH than LH which led to the suggestion that the release of FSH may be more important for maintenance of gonadal and target gland weight than that of LH. Elevation of plasma prolactin by administration of sulpiride failed to alter gonadotropin levels, testes weight or accessory organ weight. Since profound elevation or lowering of plasma prolactin did not alter the weights of testes or sex accessory organs, it appears that prolactin has little effect on these organs in adult in contrast to young rats.