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PubMed1985

Stress-induced secretion of alpha-melanocyte-stimulating hormone and its physiological role in modulating the secretion of prolactin and luteinizing hormone in the female rat.

The pattern of alpha MSH release during immobilization stress in ovariectomized rats was determined and correlated with that of plasma PRL and LH. Stress induced a marked elevation in plasma immunoreactive alpha MSH, with a time course identical to that of plasma PRL. The increment in plasma PRL was greater than that in plasma alpha MSH. Plasma LH was markedly lowered by stress. Analysis of pituitary and hypothalamic alpha MSH indicated a significant (P less than 0.05) increase in the neurointermediate lobe and anterior lobe content of alpha MSH. The alpha MSH content in the hypothalamus was lowered by stress when expressed as tissue content (P less than 0.025), although no significant differences in content in this area were detected when the results were expressed in terms of tissue protein. Stress induced a marked increase (P less than 0.01) in the median eminence levels of alpha MSH. Intraventricular (third ventricle) injection of the gamma-globulin fraction of a specific antiserum raised against alpha MSH increased basal PRL levels (P less than 0.025) and prevented the decline in plasma PRL that occurred 60 min after the onset of stress in the normal rabbit serum-injected rats. The stress-induced suppression of plasma LH was attenuated and delayed by the administration of alpha MSH antibodies. In conclusion, alpha MSH of brain origin is released during stress and is involved in lowering plasma PRL to basal levels and producing a partial suppression of plasma LH.

Animals↗
PubMed1991

Control of gonadotropin secretion in the ovine fetus. IV. Male-specific entrainment of the hypothalamic control of luteinizing hormone secretion by testosterone in the female ovine fetus.

The role of testosterone (T) in the sex-specific entrainment of hypothalamic LH regulation was studied in five castrate and four sham-castrate chronically catheterized female fetuses androgenized by the prior administration of T cypionate (200 mg, im, every 2 weeks) to pregnant ewes from 30-86 days gestation (term = 147 days). Eight female and three male castrate fetuses served as controls. After a 2-week washout period all fetuses were operated upon in utero between 106-116 days and were studied longitudinally over a 2- to 35-day period. LH pulsatility was determined from blood samples obtained every 15 min over a standard 3-h observation period and assayed for LH by RIA (NIH LH-S16 standard). LH pulse frequency in the castrate androgenized females (41 pulses in 19 observation periods; 1 pulse/1.4 h) was significantly higher than that in non-androgenized female controls (18 pulses in 28 observation periods; 1 pulse/4.7 h observation), but was similar to that in castrate males (23 pulses in 28 observation periods; 1 pulse/1.3 h). Furthermore, LH pulse frequency in the sham castrate androgenized females (26 pulses in 13 observation periods; 1 pulse/1.5 h) was comparable to that in castrate androgenized females as well as that in castrate males. The enhanced LH pulsatility in androgenized female fetuses strongly suggests that T exposure between 30-86 days results in male-specific entrainment of hypothalamic LH regulation. Moreover, the comparable enhancement of LH pulse frequency in both sham castrate and castrate androgenized female groups suggests that in the T-exposed fetus T withdrawal alone is sufficient to result in enhanced LH pulsatility. These findings strongly suggest that T of fetal testicular origin results in male-specific entrainment of hypothalamic function and may be an important feature of male neural organization in this species.

Animals↗