Biomedical subjects
Publications and source records attributed to B D Goldman.
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Treatment of male golden hamsters with melatonin injections can cause a decrease in plasma gonadotropin and Prl levels and induce testicular regression. However, administration of melatonin via subcutaneously implanted Silastic capsules can prevent short photoperiod from causing the testes to regress. In order to explain this effect of melatonin capsules, we examined plasma Prl, LH and FSH levels in pinealectomized and sham-operated hamsters in which empty or melatonin-filled Silastic capsules had been implanted. After implantation, the hamsters were transferred to a short photoperiod (5 h L:19 h D) for 9 weeks. Both pinealectomy and melatonin completely prevented the decline in plasma Prl and LH levels and in the weight of the testes and the seminal vesicles. Moreover, testicular weight and plasma Prl and LH levels were higher in pinealectomized animals given melatonin capsules than in pinealectomized animals given empty capsules. In order to obtain some indication whether melatonin may affect testicular function directly, we have examined the influenced of melatonin on the production of testosterone by hamster testes in response to hCG in vitro. Addition of 0.2, 10 or 500 ng of melatonin per ml of incubation medium had no effect on testosterone production in this system. It is concluded that melatonin capsules prevent regression of the male reproductive system in short photoperiod, most likely by preventing the decline in plasma Prl and LH levels and that these effects of melatonin are not mediated through or dependent on the pineal.
Two experiments were carried out to explore the relation between postpartum aggressive behavior in rats and other aspects of maternal behavior. In Experiment 1, nulliparous females experimentally induced to behave maternally; i.e., sensitized, failed to show elevations in aggressive responding above levels seen in untreated nulliparous controls; lactating females displayed characteristically high levels of aggression. In Experiment 2, animals in these groups were tested, along with parturient females allowed varying amounts (0 hr, 2 days, or 9 days) of postpartum exposure to young, spanning a period that is sensitive for the induction of maternal behavior. The three parturient groups responded with levels of aggression that were similar to one another and significantly higher than those seen in controls. Sensitized animals in Experiment 2 exhibited high levels of fighting; differences between these animals and those in Experiment 1 may be due to differences in both length of sensitization and ovarian cyclicity. These data indicate that the experiences of pregnancy and/or parturition prime the postparturient female to respond aggressively to an intruder later in lactation and that, unlike the initiation of pup-oriented maternal behaviors, establishment of postpartum aggression is not dependent upon pup exposure during the immediate postpartum period.
For the purpose of testing the hypothesis that the high level of aggressive behavior exhibited by postparturient rats is mediated by lactogenic hormones, hypophysectomy was performed on Day 5 postpartum, and fighting against an adult male rat was measured 4 days later. Pups were exchanged daily between hypophysectomized and sham-operated or unoperated controls animals. In Experiment 1, no differences in aggressive behavior were seen between hypophysectomized, sham-hypophysectomized, and untreated lactating animals on Day 9 postpartum. In Experiment 2, the hormonal dependence of the characteristic sensitivity to the presence of the litter in the elicitation of postpartum aggression was investigated. All animals were tested three times, on Day 9, 12, and 15 postpartum; litters were removed 4 hr prior to the second aggression test. For all groups, aggression levels were high on Day 9 with the litter present, dropped on Day 12 after removal of the litter, and showed some increment or stabilization on Day 15 with the litter again present. These experiments demonstrate that neither the expression of postpartum aggression nor the sensitivity to the presence of stimuli from the litter is directly dependent upon the hormonal milieu characteristic of lactation.
Transfer of adult male hamsters from a long to a short photoperiod causes testicular atrophy, which is accompanied by decreases in testicular LH receptors and in plasma PRL and testosterone levels. A decrease in plasma gonadotropin levels is also frequently observed. When the decline in peripheral PRL concentration is prevented by transplantation of homologous pituitary(ies) under the kidney capsule, testicular atrophy is delayed and incomplete. This appears to be due to the maintenance of testicular LH receptors by PRL secreted from the grafts and probably also to the stimulation of GSH release from the in situ pituitary. In hamsters maintained in a long photoperiod, ectopic pituitary homografts can increase testicular LH receptor levels, concentrations of testosterone and FSH in the plasma, and the weights of the testes and the seminal vesicles. In contrast to the findings obtained in rats and mice, chronic hyperprolactinemia in the male hamster does not inhibit gonadotropin release or interfere with copulatory behavior. These findings are consistent with our earlier suggestion that PRL plays an important part in the regulation of gonadal function in the male hamster but indicate that testicular atrophy in a short photoperiod cannot be explained solely by a reduction in PRL release.
The ontogeny of the pineal melatonin rhythm was determined in three rodent species. Pineal glands were obtained either during the day or during the expected peak in melatonin at night. In all species the rhythm was first detected during the second week of life. Investigations of the photic regulation of pineal melatonin revealed that light could inhibit the nocturnal increase in melatonin in all species by the end of the second week of life. These studies indicate that for these species the development of the rhythm in pineal melatonin and the development of the mechanism involved in the photic suppression of the nocturnal increase in melatonin are independent of the role the pineal gland plays in regulating reproductive function in response to changes in environmental lighting.
In the Syrian hamster, a sharp peak in pineal melatonin occurs toward the end of the dark period. In the present communication, we describe characteristics of this rhythm. First, the time of the initial increase in pineal melatonin is not altered by daily melatonin injections that induce gonadal regression. Second, the rapid decrease of pineal melatonin in the morning is not prevented by acutely extending the dark period. Third, a consistent nocturnal increase in pineal melatonin is not observed in a 20-h light, 4-h darkness lighting schedule. However, acute exposure to a longer dark period, at the appropriate time of day, allows expression of the pineal melatonin rhythm in these animals. Finally, the rhythm in pineal melatonin appears to be truly circadian and is tightly coupled to the circadian rhythm in running activity.
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Female hamsters rendered acyclic by exposure to short photoperiods (10 h light: 14 h darkness) showed diurnal surges of both LH and FSH which persisted after removal of the ovaries and adrenal glands. The reduced increase in gonadotrophin secretion after ovariectomy, typical of hamsters exposed to short days, was also not contingent upon the presence of the adrenal glands. The results demonstrate that 'supersensitivity' of the neuroendocrine axis to feedback of ovarian or adrenal steroids cannot fully account for either the daily surges of gonadotrophins or the diminished response of LH and FSH to ovariectomy in hamsters maintained on short days. It is suggested that these changes result instead from other pineal-mediated actions of short photoperiods upon the brain.
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In adult male hamsters, 2 months of exposure to a short photoperiod (5 h of light:19 h of darkness) caused testicular regression and a precipitous decline in plasma PRL, in agreement with earlier reports from other laboratories. Depressed release of PRL cannot be explained by a reduction in testicular steroidogenesis, because castration of males kept in a long photoperiod did not reduce PRL levels and administration of testosterone to males kept in a short photoperiod failed to reverse the decline in plasma PRL concentration. Treatment of such "regressed" animals with PRL, GH, or ectopic pituitary transplants stimulated growth of the testes and the accessory reproductive glands, increased the concentration of LH receptors in the testes, and elevated plasma testosterone levels. A single injection of 250 microgram PRL was sufficient to increase testicular LH binding, and chronic treatment with pituitary grafts completely reversed testicular regression. The effectiveness of exogenous PRL in stimulating testicular growth and LH receptors was significantly influenced by the timing of the injection. In some experiments, gonadotropin levels appeared elevated in animals injected with PRL, but these differences were not statistically significant. In hamsters with gonadal regression induced by exposure to a short photoperiod, daily administration of 20 microgram H and/or 150 microgram FSH had no apparent effect on testicular function. However, treatment with large doses of hCG and/or PMS gonadotropin resulted in significant stimulation of testicular growth and steroidogenesis. Chronic treatment of males maintained in a long photoperiod (14 h of light:10 h of darkness) with an inhibitor of PRL release, 2-Br-alpha-ergocryptine, resulted in a decreased weight of the testes and seminal vesicles. Administration of this inhibitor for a longer period (2 months) produced a significant increase in body weight but had little effect on testicular function. These results indicate that changes in the release of PRL (and possibly also GH) may plan an important role in mediating the effects of the photoperiod on testicular function in the golden hamster.
Pinealectomized Syrian hamsters were injected thrice daily with 25 micrograms of melatonin per injection. The injections were administered at 3-hour intervals either during the day or during the night of a photoperiodic cycle of 14 hours of light and 10 hours of darkness. After 6 weeks of treatment with melatonin during the night, both pinealectomized and intact hamsters had reduced testis weight, and pinealectomized hamsters showed decreased levels of serum gonadotropins. Injection of melatonin during the day for 7 weeks either once (75 micrograms) a day or thrice (25 micrograms per injection) daily caused a reduction in testis weight in pinealectomized hamsters. Both pinealectomized and intact females injected with melatonin thrice daily during the day became anovulatory by week 7 of treatment. These results are similar to those observed when hamsters are exposed to a short photoperiod, suggesting that melatonin may be acting as a hormone in mediating the effects of photoperiod on the reproductive system of the Syrian hamster.
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