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Long-term ovariectomized (OVX) rats were injected in the third cerebral ventricle with 5 microliter of the globulin fraction of an antiserum raised against alpha-melanocyte-stimulating hormone (alpha-MSH) or an equal volume of the globulin fraction of normal rabbit serum (NRS). Immunoneutralization of brain alpha-MSH produced an increase in the area under the secretion curve of prolactin (Prl), the amplitude of Prl pulses, and mean plasma Prl (P less than 0.01). In animals that had received two injections of NRS or anti-MSH and were subjected to a 2-min ether stress, Prl levels significantly increased within 5 minutes in the NRS-injected rats, whereas Prl levels in the antiserum-injected rats did not increase any further from the initially high baseline levels. The administration of antibodies against alpha-MSH produced a small increase (P less than 0.05) in the area under the secretion of luteinizing hormone (LH) and mean plasma LH; however, the number of LH pulses was unaffected. We conclude that endogenous alpha-MSH of central origin is a physiological neuromodulator of release of Prl and LH in the OVX rat and is involved in the stress-induced release of Prl.

The developmental pattern of hypothalamic and pituitary somatostatin and α-melanocyte-stimulating hormone (α-MSH) was studied in the rat by radioimmunoassay (RIA). Prenatally hypothalamic somatostatin was low and the first increase in content occurred on day 5 of the postnatal period. Pituitary somatostatin was undetectable prenatally and was first detected on day 6 postnatally. Pituitary somatostatin showed the same development pattern as hypothalamic somatostatin. Whole pituitaries were analyzed from the fetuses and neonates. Analysis of anterior and posterior lobes from adults revealed that all the somatostatin was in the posterior lobe. Therefore, it is believed that the somatostatin found in the glands of the younger animals was in the neural lobe. α-MSH was detected in the fetal hypothalamus as early as day 16, with a marked increase occurring on day 19 prenatally and a further increase on day 10 postnatally. Pituitary α-MSH content, readily detectable on the first day examined, i.e. day 16 of the fetal period, increased throughout development. The effect of α-MSH on the release of growth hormone in vitro from pituitaries of rats of various ages was tested. α-MSH had no effect on growth hormone release.

α-Melanocyte-stimulating hormone (α-MSH) was measured in the mediobasal hypothalamus (MH), median eminence (ME), preoptic-suprachiasmatic area (POA–SCN), anterior (AL), and posterior lobes (PL) of the pituitary gland during the gestational and postpartum periods in the rat. The content of α-MSH in the MH and POA–SCN compared to estrous levels was lower during the later days of gestation and decreased further in the MH during lactation in association with the elevated plasma prolactin (Prl). Distinct increases in the ME content of α-MSH compared to estrous levels occurred on Days 8 and 12 of the gestational period and Day 14 of the postpartum period. A significant increase in PL content of α-MSH compared to Days 5–11 and 17–20 occurred on Day 4 of gestation, and no significant changes were detected in the AP concentration of α-MSH throughout the period studied. In vitro, PLs and ALs from females on Day 4 of gestation secreted more α-MSH into the incubation medium than tissues from animals on Day 20. These results suggest that α-MSH of both brain and pituitary origin may play a role in mediating some of the physiological changes which occur during pregnancy and lactation.

To determine if LHRH might act within the brain to modify its own release, repeated blood samples were removed from conscious ovariectomized rats and minute doses of LHRH were injected into the third ventricle (3V). The effect of these injections on plasma LH and FSH was measured by radioimmunoassay (RIA). The higher dose of intraventricular LHRH (10 ng in 2 yl) induced an increase in plasma LH within 10 min after its injection. Plasma LH decreased for the next 60 min. This was followed by restoration of LH pulses characteristic of the ovariectomized rat. This dose of LHRH slightly elevated plasma FSH concentrations. In stark contrast, a 10 fold lower dose of 1 ng of LHRH injected into the ventricle resulted in a highly significant decrease of plasma LH at 10 min following injection, followed by return of LH pulsations. There was no effect on the pulsatile release of FSH. The results are interpreted to mean that at the higher dose, sufficient LHRH reached the site of origin of the hypophyseal portal vessels in the median eminence so that it diffused into portal vessels and was delivered to the gonadotrophs to induce LH release. In contrast, the lower dose provided sufficient hypothalamic concentrations of the peptide to suppress the discharge of the LHRH neurons, thereby leading to a decline in plasma LH, indicative of an ultrashort-loop negative feedback of LHRH to suppress its own release.