PROLACTIN SECRETION; ITS FUNCTION AND RELATIONSHIP TO OTHER HORMONES IN THE MALE RAT

Prolactin is secreted by the anterior pituitary and is under the control of a secretion from the hypothalamus called prolactin inhibitory factor (PIF) which is directed to the pituitary by way of the median eminence. Prolactin secretion by the in site pituitary is inversely proportional to the secretion of PIF. The influence of the PIF is lost or greatly reduced when the pituitary is transplanted to an exogenous site which results in a marked increase in prolactin secretion. In the female rat there is a prolactin surge on the afternoon of proestrous. In the pseudopregnant and pregnant rat, prolactin is secreted according to a diurnal rhythm and is responsible for maintenance of the corpus luteum and progesterone secretion. Prolactin in combination with progesterone promotes growth of the alveolar lobules in the mammary glands and after parturation, prolactin along with insulin and adrenal corticoids initiates and maintains milk secretion. In the male rat, prolactin in combination with LH stimulates testosterone secretion and in combination with testosterone stimulates growth of secondary sex tissues, however in the male rat these effects appear to be somewhat less than critical. Many aspects of prolactin in the male have not been investigated including the 24-hour secretory pattern, the effects of excessive or deficient serum prolactin concentrations in adults and the importance of prolactin to the normal development of immature male rats. The first manuscript in this thesis investigated the secretory pattern of prolactin throughout a 24-hour period. In addition, the secretory pattern of other tropic hormones and testosterone were investigated primarily to determine if any obvious relationships exist between the secretion of prolactin and these other hormones. The second study investigated prolactin function by monitoring the effects of chronic prolactin deficiency on the development of secondary sex structures and on the secretion of other hormones. Prolactin deficiency was initiated and maintained by periodic injections of an antiserum to rat prolactin. The third study was an investigation to determine if the sequence of events leading to the diurnal prolactin rhythm, which was discovered in the first study, was dependent on the presence of the adrenal glands

Steroid Metabolism in Superovulated Rats with Transplanted Pituitaries Following Hypophysectomy

Ovulation and luteinization were artificially induced in prepubertal rats by administration of 50 IU PMS followed 60±5 hours later by 25 IU HCG. Hypophysectomy, pituitary transplantation, and treatment with anti-LH serum were used to investigate the nature of hypophyseal involvement in the precursor and steroid metabolism of the luteinized ovary. Plasma and ovarian levels of progesterone and 20α-OH-pregn-4-ene-3-one and ovarian levels of cholesterol and esterified cholesterol were determined. The uptake of 14C-acetate into these compounds both in vivo and in vitro was also determined. Hypophysectomy was shown to cause a rapid reduction in plasma and ovarian steroid levels. However, hypophysectomized animals that were provided with pituitary transplants maintained steroids at intact levels even after repeated injection with anti-LH serum. This indicates that LH is not directly involved with steroid synthesis. Ovarian cholesterol and esterified cholesterol levels were greatly depressed by hypophysectomy. The presence of transplanted pituitaries in hypophysectomized animals resulted in a partial recovery of precursor levels. This recovery did not take place in transplanted animals that were treated with anti-LH serum. These results strongly suggest that transplants do produce some LH, that LH is directly involved in maintaining precursor pools, but that high precursor pools are not critical in maintaining steroid production in the superovulated rat. The uptake of 14C-Acetate into steroids and steroid precursors was greatly increased following hypophysectomy but hypophysectomized animals that had received pituitary transplants did not show this increase unless they were treated with anti-LH serum. It is apparent from this investigation that the uptake of acetate is not proportional to the magnitude of precursor or steroid formation. A compatible explanation would be that LH stimulated the production of acetate, perhaps by enhancing glycolysis. This would dilute the specific activity of the labeled acetate, resulting in a reduced uptake of the label into steroid precursors and steroids