Infusion of testosterone into the testicular artery, at concentrations comparable to those that occur in the testicular vein in situ, inhibited LH-stimulated testosterone secretion by rat testes perfused in vitro. This inhibition was rapid and dose responsive. In contrast to testosterone, intra-arterial infusion of 5 alpha-androstan-3 alpha, 17 beta-diol, corticosterone and androstenedione failed to inhibit testosterone secretion. The inhibition of testosterone secretion by intra-arterial infusion of testosterone was reversed by either cessation of testosterone infusion or the simultaneous addition of androstenedione to the artificial perfusion medium. Taken together, these results showed that LH-stimulated testosterone secretion by in vitro perfused rat testes was inhibited by a short-loop negative feedback of testosterone.

The natural estrous cycle of captive Senegal galagos was analyzed from daily records of 11 cycling females for 18 months, and induction of vaginal estrus and ovulation by gonadotropins and estrogen were examined in 9 females. No seasonal trend in cycling was indicated, as at least 5 of the 11 cycling females exhibited vaginal estrus during each month. Cycle lengths and duration of estrus were consistent for each female but varied significantly among females. Individuals’ average cycle lengths ranged from 29.2 ± 0.8 to 39.3 ± 3.4 days, and duration of estrus from 4.8 ± 0.2 to 6.7 ± 0.4 days. Vaginal estrus was induced by PMSG and PMSG-HCG combinations, and by estradiol. The gonadotropins also induced growth and ovulation of more than one follicle.

First estrus is advanced in female house mice exposed to an adult male and delayed in those housed in groups. Experiments were conducted to explore possible mechanisms by which the hypothalamus integrates these puberty-regulating social signals. Female mice weaned at 21 days of age were placed in groups of 8 (G8JF), a juvenile female with a juvenile male (JFJM) or juvenile female with an adult male (JFAM). All females were ovariectomized on day 28 and sacrificed on day 29. There was no significant difference between treatments in the postovariectomy rise in LH. Next, female mice were weaned, assigned to G8JF, JFJM or JFAM treatments and ovariectomized on day 22. Females were sacrificed on day 29, 3 h after injection with either 1.0 µg of estradiol, or vehicle. Estradiol significantly suppressed LH in all three treatments, with no differences between treatments. Two-way ANOVA (social treatment × estradiol treatment) revealed no differences or interactions in brain catecholamines as a result of estradiol injection. The G8JF treatment significantly increased norepinephrine, (NE), dopamine (DA) and its metabolite 3,4-dihydroxy-phenylacetic acid in the mediobasal hypothalamus (MBH), and the 3-methoxy-4-hydroxy-phenylglycol/NE ratio in the preoptic area (POA). In the final experiments, isolate prepubertal female mice were treated with either water or male urine (MU) on the oronasal groove. Eight days of MU treatment resulted in significant uterine growth, however there were no differences in serum LH, POA or MBH catecholamines or POA and median eminence LHRH. One hour after application of MU, serum LH was significantly elevated, however, there were no differences in accessory olfactory bulb catecholamines. These results suggest that the mechanism by which male and grouped female exposure alters first estrus may not involve changes in sensitivity to estradiol negative feedback. Grouping may delay first estrus through the negative effects of DA on the LHRH system in the MBH. We observed no differences that might help to explain how male exposure causes LH release.

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