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.

We have examined testicular and pituitary function in inbred CD-F rats and DBA/2J mice with chronic hyperprolactinemia induced by grafting 4 anterior pituitaries from adult females of the same strain under the kidney capsule. Eight rats were given pituitary isografts and 9 were sham-operated; blood samples were collected at 4-7 week intervals, and the animals were killed 6 months later. One month after surgery, PRL levels in grafted rats were elevated (348 +/- 15 vs. 94 +/- 11 ng/ml; P less than 0.001), LH levels were depressed (16 +/- 3 vs. 59 +/- 9 ng/ml; P less than 0.001), but T levels were not affected (1.0 +/- 0.1 vs. 1.1 +/- 0.2 ng/ml). The elevated PRL levels in grafted animals did not decline during the subsequent 5 months, while LH levels increased slightly, and T levels remained indistinguishable from those in the controls. At the time of autopsy, FSH levels were reduced in grafted rats (230 +/- 40 vs. 501 +/- 108 ng/ml; P less than 0.05). Multiple pituitary isografts did not affect the weight of the testes or the ventral prostate, but increased the weight of the seminal vesicles (P less than 0.001). In 11 mice examined 5.5 months after receiving pituitary isografts, plasma PRL levels were dramatically elevated (330 +/- 35 vs. 27 +/- 2 ng/ml; P less than 0.001), but plasma T levels and testicular weight were not different from those observed in 12 sham-operated controls. The weight of the seminal vesicles in grafted mice was increased (P less than 0.01). In both rats and mice, chronic hyperprolactinemia did not affect plasma testosterone levels or testes weight and increased seminal vesicle weight.

Male house mice paired with a normal female for 1 week do not have higher plasma testosterone levels than do males that remain in all-male groups, but paired males have markedly elevated testosterone levels 30 to 60 minutes after the resident female is replaced by another female. Elevation of testosterone levels in these males is similar to that in isolated males paired with a female, does not depend on copulation with the strange female, occurs under housing conditions that permit continuous exposure to the odors of other females and males, and does not occur when the resident female is replaced by another male for 30 to 60 minutes. The elevation thus appears to be a specific endocrine response to an encounter with a strange female. These results, along with previous findings suggesting that strange males affect endocrine function in females, indicate that bisexual encounters are likely to produce endocrine changes in members of both sexes.

No abstract

Themain psychoactive component of marihuana, delta-9-tetrahydrocannabinol (THC) was injected into the 3rd cerebral ventricle. A single dose of THC (2 µl of 1(HM) decreased serum LH temporarily but did not alter serum follicle-stimulating hormone (FSH) levels. The mediobasal hypothalamic (MBH) luteinizing hormone-releasing hormone (LHRH) content was elevated by 30 min after the injection. The elevation persisted for 1 h. Then, the LHRH content returned towards the preinjection level. In contrast, the LHRH in the organum vasculosum of the lamina terminalis did not change after a single dose of THC. The results indicate that THC alters pituitary LH release by inhibiting the release of LHRH which then increases in the MBH by continued synthesis or transport from rostral areas. In addition, the data support the existence of an FSH releasing factor, the release of which is not suppressed by this dose of THC. THC did not alter the release, storage or responsiveness to LHRH of cultured anterior pituitary cells, which further supports the view that its principal site of action is on the hypothalamus.