Genetic and phenotypic influences on copulatory plug survival in mice.

Across a diversity of animals, male seminal fluid coagulates upon ejaculation to form a hardened structure known as a copulatory plug. Previous studies suggest that copulatory plugs evolved as a mechanism for males to impede remating by females, but detailed investigations into the time course over which plugs survive in the female's reproductive tract are lacking. Here, we cross males from eight inbred strains to females from two inbred strains of house mice (Mus musculus domesticus). Plug survival was significantly affected by male genotype. Against intuition, plug survival time was negatively correlated with plug size: long-lasting plugs were small and relatively more susceptible to proteolysis. Plug size was associated with divergence in major protein composition of seminal vesicle fluid, suggesting that changes in gene expression may play an important role in plug dynamics. In contrast, we found no correlation to genetic variation in the protein-coding regions of five genes thought to be important in copulatory plug formation (Tgm4, Svs1, Svs2, Svs4 and Svs5). Our study demonstrates a complex relationship between copulatory plug characteristics and survival. We discuss several models to explain unexpected variation in plug phenotypes.

Ventromedial hypothalamic mediation of photoperiodic gonadal responses in male Syrian hamsters.

Short day lengths induce testicular regression in seasonally breeding Syrian hamsters. To test whether the ventromedial hypothalamus is necessary to maintain reproductive quiescence once testicular regression has been achieved, photoregressed male hamsters were subjected to lesions of the ventromedial hypothalamus (VMHx), pinealectomy (Pinx), or sham operation (Sham). VMHx hamsters underwent accelerated gonadal recrudescence compared to Pinx and Sham hamsters. Recovery of prolactin concentrations (PRL) to values characteristic of long-day hamsters was hastened in the VMHx animals compared to Sham hamsters. Concentrations of follicle stimulating hormone (FSH) increased prematurely in both the VMHx and Pinx animals, beginning a few weeks after surgery. By the time the gonads had undergone recrudescence and the hamsters were refractory to melatonin, PRL and FSH concentrations had returned to baseline long-day values in all groups; there was no evidence of hypersecretion of either hormone in any of the animals with lesions. Melatonin concentrations of VMHx hamsters did not differ from those of sham-operated animals, but because only a single determination was made, it remains possible that VMH damage altered the duration of nightly melatonin secretion. An intact VMH appears to be essential for the continued maintenance of reproductive suppression induced by exposure to short day lengths; these and earlier findings suggest that the VMH-dorsomedial hypothalamic complex mediates regression of the reproductive apparatus during decreasing day lengths of late summer and early autumn and also is necessary to sustain regression during the winter months.

Effects of photoperiod duration and melatonin signal characteristics on the reproductive system of male Syrian hamsters.

Three experiments tested effects of photoperiod and the pineal hormone melatonin (MEL) on reproductive function among male Syrian-hamsters. In Experiment 1, hamsters were exposed for 32 weeks to 1 of 4 short photoperiods which varied in duration (11.5 L; 10 L; 8 L; 6 L). A fifth group was shifted from 11.5 L to 6 L after 6 weeks. Shorter photoperiods were associated with more rapid regression of the testes, but all groups eventually regressed to the same extent. In contrast, the temporal profile of testicular recrudescence, expressed as males became photorefractory, was not significantly different between groups. A decrease in photoperiod from 11.5 L to 6 L after 6 weeks did not delay the onset of recrudescence. The 11.5 L group was subdivided at week 32 and transferred to either 13 L or 16 L for the next 8 weeks to break photorefractoriness. Upon subsequent exposure to 8 L, both subgroups regressed their testes in similar fashion over weeks 40-52, indicating that the two long photoperiods were equally effective in breaking photorefractoriness. Nevertheless, FSH and prolactin were more consistently suppressed in the 16 L group following the switch to 8 L. Experiment 2 tested whether differing durations of MEL, administered s.c. each night for 9 weeks, elicit graded rates of reproductive regression in pinealectomized males. Testicular regression was more rapid in the group receiving MEL for 12 h than it was in the group receiving MEL for 8.5 h, thus supporting the hypothesis that the faster rates of testicular regression in the shorter photoperiods of Experiment 1 were due to their concomitant longer durations of nightly MEL secretion. Experiment 3 tested the hypothesis that rates of testicular regression in males receiving exogenous MEL would be affected by their prior photoperiodic history. Males were exposed to 18 L or 14 L for 7 weeks, then pinealectomized and administered 9.5 h MEL infusions s.c. each night for 9 weeks. In contrast to predictions, photoperiodic history had only transitory effects on MEL-induced testicular regression. Although the differences in MEL duration that accompany different short photoperiods have reproductive consequences (Experiment 1), the extent to which MEL duration expands during the transition from stimulatory to inhibitory photoperiods appears to be a less significant variable (Experiment 3).

Effect of photoperiod on neural estrogen and progestin receptor immunoreactivity in female Syrian hamsters.

This study explored the possibility that reduced behavioral responsiveness to estradiol and progesterone in female Syrian hamsters exposed to a short photoperiod is associated with a reduction in the concentration of neural steroid receptors. The effects of long and short photoperiod (LP; SP) exposure on steroid receptor immunoreactivity were examined in the ventromedial hypothalamus (VMH), medial tuberal region (mTu), medial preoptic area (mPOA), medial nucleus of the amygdala (mAMYG), and the arcuate nucleus (ARC) of ovariectomized hamsters. In Experiment 1, exposure to SP for ten weeks attenuated the lordosis response following sequential treatment with estradiol and progesterone. In a separate group of animals not given hormones, SP decreased the staining intensity of estrogen receptor immunoreactive (ERIR) cells in the mPOA while increasing the number of detectable ERIR cells in part of the mAMYG. In Experiment 2, SP diminished the lordosis response as it did in Experiment 1. One week later, the same females were administered estradiol systemically to induce progestin receptors (PR). Animals housed in SP showed significantly reduced progestin receptor immunoreactivity (PRIR) in the VMH, mTu, mPOA, mAMYG, and ARC. Experiment 3 examined whether the results of Experiment 2 might have been influenced by photoperiodic effects on peripheral metabolism of estradiol. Among hamsters housed in LP or SP, PRs were induced by estradiol implanted unilaterally in the medial basal hypothalamus, thus bypassing possible photoperiodic effects on peripheral estradiol availability. This treatment resulted in significantly fewer cells with detectable PRIR in the VMH and mPOA of SP females, suggesting that the photoperiodic influences on PR induction observed in Experiment 2 do not depend on alterations in the peripheral availability of estradiol.

Food deprivation and the facilitatory effects of estrogen in female hamsters: the LH surge and locomotor activity.

Two experiments investigated short-term food deprivation effects on neuroendocrine processes influenced by estrogen. These studies were prompted by prior work indicating that food deprivation increased the number of immunocytochemically identified cells containing estradiol receptors in the medial preoptic area of ovariectomized female hamsters. Presumably, this is one way that changes in metabolic fuel availability might alter the responsiveness of one or more systems to estradiol. The purpose of this study was to investigate two effects of estradiol that might be affected by food deprivation; these were 1) the positive feedback effects of estradiol on the luteinizing hormone (LH) surge, and 2) the facilitating effects of estradiol on locomotor activity. In Experiment 1, ovariectomized hamsters were administered estradiol, before or after 48 h of food deprivation. Two days after hormone treatment, blood was obtained by cardiac puncture, once in the morning (1100 h) and twice during the afternoon (1600-1800 h). These times were chosen to best characterize the magnitude of the LH surge. Food deprivation enhanced the amplitude of the LH surge in response to estradiol when this treatment preceded, but not when it followed, the administration of estradiol. However, there was variability in the dose of estradiol at which this effect of food deprivation occurred. In Experiment 2, the locomotor (running wheel) activity of two groups of gonadally intact female hamsters was quantified; one group was tested during the early (days 1 + 2; low estradiol) part of the estrous cycle, and the other group was tested during the late (days 3 + 4; high estradiol part of the estrous cycle. In both groups, testing was performed first under ad lib feeding conditions and again during 48 h of food deprivation. On average, the days 3 + 4 group was more active than the days 1 + 2 group, reflecting their differing levels of endogenous estradiol. Food deprivation significantly increased locomotor activity, independently of the stage of the estrous cycle during which it was imposed. These results are discussed in terms of the influence that altered estradiol receptor expression in the medial preoptic area might play in generating the effects we observed following short-term food deprivation.

AP lesions block suppression of estrous behavior, but not estrous cyclicity, in food-deprived Syrian hamsters.

Food deprivation inhibits ovulatory cycles and estrous behavior in Syrian hamsters. Lesions of the area postrema (AP) prevented the suppression of estrous behavior in food-deprived hamsters, but they did not prevent the suppression of estrous cyclicity or the increase in running-wheel activity caused by food deprivation. Food deprivation or treatment with pharmacological inhibitors of glycolysis and fatty acid oxidation decreased estrogen-receptor immunoreactivity (ERIR) in the ventromedial hypothalamus (VMH), increased ERIR in the arcuate nucleus (Arc) and the posterior parvicellular paraventricular nucleus (PaPo), but had no effect on ERIR in the posterodorsal medial amygdala or the anterior parvicellular paraventricular nucleus. Lesions of the AP prevented the food deprivation-induced decrease in VMH ERIR and the increase in Arc ERIR, but they did not prevent the increase in ERIR in the PaPo. Thus, whatever physiological cues are produced by food deprivation, an intact AP is required for their transmission to the neural circuits controlling estrous behavior, VMH ERIR, and Arc ERIR. The AP is not essential for transmission of this information to the neural circuits controlling estrous cyclicity, running-wheel activity, or PaPo ERIR.