Adrenal function in female rats before puberty: the effects of gonadectomy

The following study was designed to test whether the change in the amplitude of the adrenal rhythm and the response to stress seen at puberty in female rats is dependent upon stimulation of the adrenal system by gonadal steroids. Rats were gonadectomized either at two days of age or at 21 days of age and periodic blood samples were taken by cardiac puncture and assayed for corticosterone (B) by a fluorometric procedure. Ovariectomy at weaning age (21 days) had no effect on adrenal function until the time of normal puberty onset. In intact animals, a rise in resting levels of corticosterone and an increase in the incremental response to ether stress was noted at 35 days of age. (Puberty in females was 35.3 ± 1.2 days as indicated by vaginal opening). Ovulation occurred the following day in 9/10 rats. Gonadectomy at two days of age had essentially the same effect as later gonadectomy in females. By 70 days of age, resting corticosterone values and stress responses in gonadectomized females reached levels similar to intact females. It is concluded that an independent adrenarche can occur in females but that gonadal steroids present at the time of puberty modulate the timing of this process.     

Reproductive aspects in female rats exposed prenatally to hydrocortisone

We investigated the effects of hydrocortisone during the prenatal period and its later repercussion on reproductive aspects of female rats. Pregnant rats were treated (s.c.) with hydrocortisone acetate, at 1.5 mg/day on the 17th, 18th, and 19th days of pregnancy. Although the present study was not intended to identify mechanisms of toxicity, the treatment with hydrocortisone in the last period of pregnancy presented no signs of toxicity. The efficacy of the hydrocortisone in reducing the adrenal wet mass and plasma corticosterone levels immediately after delivery in both the treated mothers and in respective pups at birth may indicate impairment of the hypothalamus-pituitary-adrenal axis. In addition, the treatment with hydrocortisone did not interfere in the development of the female descendants until puberty. However, it affected the estrous cycle and fertility. Probably, the prenatal exposure to corticosteroids had altered at least partially the hypothalamus-pituitary-gonadal axis, resulting in the damages observed in adult life. These results indicate that the use of the hydrocortisone at a dose that apparently does not endanger the neonate led to undesirable effects in the adult reproductive phase, resulting in later deleterious alteration of the reproductive physiology in female rats.     

Reproductive function and sexual behaviour in female rats exposed to immobilization stress or ACTH injections during gestation

Pregnant primiparous rats were exposed to low immobilization stress or ACTH injections (one unit) throughout pregnancy. We measured the following parameters in the female offsprings: puberty (vaginal opening and first oestrous), oestrous cycle and sexual behaviour. Compared to the controls, female sexual receptivity measured by means of lordosis and the lordosis quotient (LQ) increased in both the experimental groups, but the puberty parameters of the offspring did not alter.     

Reproductive function in aged female chimpanzees.

Reproductive function was evaluated in ten female chimpanzees (Pan troglodytes) aged 35-48 years. Forty-eight years is the longevity record for the chimpanzee. Data on cycle frequency and duration was available for seven animals. Most were cycling regularly until death, and all had experienced at least one menstrual cycle within one year of death. After exclusion of periods when the animals were pregnant or in postpartum amenorrhea, the mean cycle frequency (+/- standard error)/year was 9.54 +/- 0.20 in seven animals aged 15-25 (432 cycles analyzed) compared to 8.6 +/- 0.76 in the same animals at age 35 + years (405 cycles analyzed); this effect approached significance (p = 0.072, Mann-Whitney U-test). Cycle length of 16 cycles in each of seven animals aged 15-25 was 32.23 +/- 0.38 days. The same animals when aged over 35 had mean cycle lengths of 35.59 +/- 0.73. This difference was not significant, although cycle lengths clearly increased with age in some individual animals. In five aged animals for which mating data was available, appropriate exposure to a male occurred in 52 cycles, but only two pregnancies occurred; one pregnancy resulted in a live birth at age 38, the other in a stillbirth at age 40. This conception rate was 3.85% compared with 20% in the same animals aged 15-25. These data suggest greatly reduced fertility after age 35, although menstrual cycle frequency remained high. The persistence of menstrual cyclicity until death, which occurred due to natural causes at latest in the fifth decade, is in striking contrast to the human female in which menopause occurs in the fifth decade and death is often postponed for several more decades.     

Dietary fish oil delays puberty in female rats.

Marine oils contain eicosapentaenoic acid, a fatty acid that competes for cyclooxygenase and reduces the synthesis of dienoic prostanoids including prostaglandin E2 (PGE2). Since PGE2 plays an important role in the estrogen-stimulated release of hypothalamic GnRH on proestrus, it was postulated that a diet containing fish oil would delay first ovulation through inhibitory effects on GnRH release. Thirty, 22-day-old female Sprague-Dawley rats were fed a diet containing fish oil ad libitum. Controls were pair-fed an identical diet with the substitution of safflower oil as the dietary fat. All rats were killed on the morning of first metestrus after vaginal opening and the display of an estrous smear(s). Fish oil feeding did not affect growth as indicated by the lack of an observed effect on body weights or femur lengths. On the other hand, pituitary, ovarian, and uterine weights were significantly lower in the rats fed fish oil (p < 0.001). The age at first estrus of the rats fed fish oil was significantly increased compared with the controls (42.9 +/- 1.0 vs. 36.1 +/- 0.3 days; p < 0.001), whereas the number of rats with corpora lutea (CL), as well as the number of CL per ovary (2.3 +/- 0.4 vs 4.8 +/- 0.6 for controls; p < 0.001) was significantly reduced by fish oil feeding. GnRH concentration in the preoptic area/hypothalamus was significantly increased in the fish oil-fed rats (21.4 +/- 4.0 pg/mg vs. 7.6 +/- 2.2 pg/mg for controls; p < 0.01); radioimmunoassable hypothalamic PGE2 was concomitantly reduced (p < 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)     

Peripubertal exposure to male odors influences female puberty and adult expression of male-directed odor preference in mice

Testosterone-dependent olfactory signals emitted by male are well known to accelerate female puberty in mice (Vandenbergh effect). However, it remains unclear whether these chemosignals also influence adult expression of male-directed odor preference. Therefore, we exposed female mice to intact or castrated male bedding (vs clean bedding as control) during the peripubertal period (postnatal day (PD) 21–38) and measured male-directed odor preference in adulthood. At PD45 or PD60, females exposed to intact male odors, and thus showing puberty acceleration, preferred to investigate odors from intact males over females or castrated males. Females exposed to castrated male odors did not show puberty acceleration but preferred male (intact or castrated) over female odors. Finally, control females did not show any odor preference when tested at PD45, although a preference for male odors emerged later (PD60). In a second experiment, females that were exposed to intact male odors after pubertal transition (PD36–53) also preferred intact male over castrated male odors. In conclusion, our results indicate that peripubertal exposure to male odors induced early expression of male-directed odor preference regardless of puberty-accelerating effect and that induction of male-directed odor preference is not specific to the peripubertal period.     

Food deprivation affects reproduction in adult female mice (Mus musculus) and the age of puberty for their female progeny

Three experiments were designed to test the effects of food deprivation during various phases of the reproductive cycle on fertility and fecundity of the dams and on the age of sexual maturation and body growth of their female progeny. Food deprivation consisted of removal of all food every other day. Animals were deprived of food either during the period prior to pairing, during the period between pairing and conception or during gestation. Both fertility and fecundity were affected by food deprivation in some, but not all manipulations. The female progeny of food-deprived females reached puberty significantly later than the progeny of non-deprived dams when the food deprivation occurred during the week prior to pairing and up until successful insemination after pairing with a fertile male, but not when food deprivation occurred at other times during the reproductive cycle. Body growth did not differ in the daughters of food-deprived dams across the treatments for any of the experiments.     

Effects of acute stanozolol treatment on puberty in female rats

The effects of anabolic-androgenic steroid (AAS) abuse on the onset of puberty in female adolescents are largely unknown. This study assessed the acute effects of one AAS, stanozolol, on pubertal onset in the female rat. A single injection of stanozolol (5 mg/kg) on Postnatal Day (PN) 21 advanced vaginal opening but did not alter the onset of vaginal estrus. Higher doses of stanozolol treatment (10 and 25 mg/kg) also advanced vaginal opening but had no effect on vaginal estrus. The advancement of vaginal opening by stanozolol (5 mg/kg) was prevented by the concomitant administration of the pure antiestrogen ICI 182,780 (1 mg/kg) on PN20-22. Administration of the androgen receptor antagonist flutamide (10 mg/kg twice daily) on PN20-22 had no effect on the advancement of vaginal opening by stanozolol. Stanozolol treatment also advanced vaginal opening in ovariectomized rats. Perivaginal injections of a low dose of stanozolol (0.05 mg) on PN21 and PN23 also advanced vaginal opening. These results suggest that stanozolol is acting directly at estrogen receptors in the vaginal epithelium to advance vaginal opening and that prepubertal stanozolol treatment does not induce true precocious puberty.     

Reproductive axis response to repeated lipopolysaccharide administration in peripubertal female rats

Immune system disorders are often accompanied by alterations in the reproductive axis. Several reports have shown that administration of bacterial lipopolysaccharide (LPS) has central inflammatory effects and activates cytokine release in the hypothalamus where the luteinizing hormone releasing hormone (Gn-RH) neurons are located. The present study was designed to investigate the effect of repeated LPS administration on the neuroendocrine mechanisms of control of the reproductive axis in peripubertal female rats (30-day-old rats). With this aim, LPS (50 μg/kg weight) was administered to the animals during 25, 27 and 29 days of age and sacrificed on 30 day of life. Gn-RH, γ?amino butyric acid (GABA) and glutamic acid (GLU), two amino acids involved in the regulation of Gn-RH secretion, hypothalamic content were measured. LH and estradiol serum levels were also determined and the day of vaginal opening examined. The results showed a significant increase in Gn-RH and GLU content (p?<?0.0001), shared by a reduction of GABA one (p?<?0.0001). LH and estradiol serum levels were decreased (p?<?0.01, p?<?0.001) and delay in the day of vaginal opening was also observed in treated animals. Present results show that repeated LPS administration impaired reproductive function, modifying the neuroendocrine mechanisms of control of the axis in peripubertal female rats.     

Immune activation decreases sperm viability in both sexes and influences female sperm storage

All animals are under the constant threat of pathogenic infection. However, little is known regarding the influence of acute infection on sperm viability, particularly in female insects. This information is crucial for our understanding of mating and immune system coevolution, considering that females store sperm and serve as the site of sperm competition. Using the fruitfly, Drosophila melanogaster, we examined the influence of infection on sperm viability and storage. Twenty-four hours after haemocoel inoculation with a pathogen mimic (peptidoglycan, PGN) both sexes exhibited reduced sperm viability, indicating that systemic immune activation played a significant role in gamete survival. Surprisingly, sperm death did not appear to result from a reproductive-immune system trade-off, considering that sperm survived 24 h in vitro once removed from their somatic resources. Instead, our results are most consistent with death owing to immune effector collateral damage. We also examined the potential for sexually transmitted pathogens to influence sperm storage. Females mated with 'infected' males (created by dipping genitalia into a PGN solution) exhibited a higher proportion of empty sperm stores 48 h after mating compared to their controls. Remarkably, these data indicate that females may increase their fitness by removing 'infected' ejaculates from storage over time.     

Reproductive experience modifies dopaminergic function, serum levels of prolactin, and macrophage activity in female rats

Reproductive experience (RE), i.e. pregnancy and lactation, induces physiological changes in mammals. Recent data show that neuroimmune interactions are modulated by a diversity of events involving neurotransmitters and neuropeptides. These molecules, particularly dopamine (DA), were reported to mediate the relevant cross talk between immune and neuroendocrine systems. Moreover, DA-mediated regulation of leukocyte function is a reasonable approach to investigate the DA-operated regulatory switch for immune-competent cells, such as macrophages. Therefore, the goals of the present study were to determine the effects of RE on: (1) dopaminergic function through hypothalamic levels of DA, dihydroxyphenylacetic acid (DOPAC), homovanilic acid (HVA), serotonin (5-HT), and 5-hydroxyindole acetic acid (5-HIAA); (2) basal levels of circulating prolactin (PRL); and (3) activity of peritoneal macrophage (phagocytosis and oxidative burst). A total of 16 adult (200-250 g) female Wistar rats were used, divided in two groups: nulliparous and primiparous. Approximately 2-3 weeks after weaning pups from the primiparous group, both groups of rats were tested. The findings indicate that: (1) DOPAC concentrations, DOPAC/DA and HVA+DOPAC/DA ratios decreased in primiparous rats as compared to virgin rats, (2) primiparous rats showed significantly lower serum PRL levels, and (3) phorbol miristate acetate (PMA)-induced oxidative burst was decreased in peritoneal macrophage from primiparous rats as compared to virgin rats. To test the possible positive correlation between serum levels of PRL and the intensity of oxidative burst by peritoneal macrophage, an extra experiment was done with adult virgin female rats treated with domperidone, an antagonist of DA receptors. Domperidone-treated animals showed increased serum levels of PRL and simultaneous increase in peritoneal macrophage oxidative burst. Thus, suggesting an indirect participation of hyperprolactinemia, induced by this treatment in peritoneal macrophage activity of female rats. These results suggest that a previous RE can modulate the activity of dopaminergic hypothalamic systems, while decreasing PRL serum levels and the oxidative burst of peritoneal macrophage. The neurochemical and hormonal RE-induced changes correlate with the immune alterations.     

The emergence of gonadal hormone influences on dopaminergic function during puberty

Adolescence is the developmental epoch during which children become adults—intellectually, physically, hormonally and socially. Brain development in critical areas is ongoing. Adolescents are risk-taking and novelty-seeking and they weigh positive experiences more heavily and negative experiences less than adults. This inherent behavioral bias can lead to risky behaviors like drug taking. Most drug addictions start during adolescence and early drug-taking is associated with an increased rate of drug abuse and dependence.The hormonal changes of puberty contribute to physical, emotional, intellectual and social changes during adolescence. These hormonal events do not just cause maturation of reproductive function and the emergence of secondary sex characteristics. They contribute to the appearance of sex differences in non-reproductive behaviors as well. Sex differences in drug use behaviors are among the latter. The male predominance in overall drug use appears by the end of adolescence, while girls develop the rapid progression from first use to dependence (telescoping) that represent a female-biased vulnerability. Sex differences in many behaviors including drug use have been attributed to social and cultural factors. A narrowing gap in drug use between adolescent boys and girls supports this thesis. However, some sex differences in addiction vulnerability reflect biologic differences in brain circuits involved in addiction. The purpose of this review is to summarize the contribution of sex differences in the function of ascending dopamine systems that are critical to reinforcement, to briefly summarize the behavioral, neurochemical and anatomical changes in brain dopaminergic functions related to addiction that occur during adolescence and to present new findings about the emergence of sex differences in dopaminergic function during adolescence.     

The selenium intake of the female chicken influences the selenium status of her progeny

The primary purpose of this study is to determine the extent to which the effects of dietary supplementation of the female chicken with selenium (Se) continue into the next generation. An additional aim is to compare the relative effectiveness of pre-hatch (from the hen's diet) with that of post-hatch (from the progeny's diet) supplementation with Se on the Se status of the chick during the first 4 weeks of post-hatch life. Hens were maintained on control or Se-supplemented diets, respectively containing 0.027 and 0.419 μg Se/g of feed. The high-Se diet elevated the Se content of the hens' eggs by 7.1-fold. At hatch, the concentrations of Se in the liver, breast muscle and whole blood of the chicks originating from the high-Se parents were, respectively, 5.4-, 4.3- and 7.7-fold higher than the values in the chicks of the low-Se parents. When the offspring from the two parental groups were both maintained on the low-Se progeny diet, the tissue Se concentrations in chicks originating from the high-Se hens remained significantly higher for 3–4 weeks after hatching, compared with the values in chicks from the low-Se hens. Similarly, tissue glutathione peroxidase activity remained significantly higher in chicks from the high-Se hens for 2–4 weeks post-hatch. Thus, the effects of maternal Se supplementation persist in the progeny for several weeks after hatching. However, when chicks hatching from low-Se eggs were placed on a high Se diet, their tissue Se concentrations at 7 days of age were markedly higher than the values in chicks from high-Se eggs placed on the low-Se diet.