Hormones and Behavior最新文献

Kisspeptin (Kp), a potent regulator of the hypothalamic-pituitary-gonad axis, was recently shown to be involved in partner preference and sexual receptivity in females. Interestingly, Kp and its receptor (Kiss1r) are expressed in brain regions involved in the reward and motivation of reinforcing behaviors. Therefore, in the present study, we designed 3 experiments to determine the participation of Kp in female sexual behavior and the positive affective (PA) reward state induced by paced mating (PM). In all experiments, we used sexually naïve ovariectomized Wistar female rats primed with estradiol benzoate (EB, 2.5 μg/rat) 48 h before behavioral tests. In experiment 1 (n = 9), we tested the effect of Kp on PM. We demonstrated that Kp-10 (14 nmol) induced similar levels of receptivity to treatment with EB + progesterone and facilitated PM by reducing the return latency after intromissions. In experiment 2 (n = 8), we evaluated the effect of p234 penetratin, a Kiss1r antagonist, on PM. The administration of p234 in doses of 7.5 nmol and 15 nmol reduced the mean lordosis intensity and increased mount and intromission return latencies. Finally, in Experiment 3, we tested the capacity of Kp to induce a PA state or the antagonist to block the reward state induced by PM. Kp-10 (7 and 14 nmol) induced a clear conditioned place preference. This reward state and that produced by PM were blocked by p234 (15 nmol). Our findings underscore the critical role of Kp in modulating female sexual behavior and the PA state associated with PM, highlighting its potential to enhance sexual motivation.

The aim of the present study was to investigate the role of ovarian hormones on dopaminergic regulation of prepulse inhibition (PPI), a measure of sensorimotor gating deficient in schizophrenia and other psychiatric illnesses. Either in adulthood (11 weeks of age) or adolescence (5 weeks of age), female mice underwent ovariectomy (OVX) and were implanted with 17β-estradiol, progesterone, or a combination of these hormones. All mice were tested in adulthood for the acute effect of the dopamine receptor agonist, apomorphine, on PPI. Apomorphine treatment reduced PPI in intact mice and this effect was blocked after OVX in adulthood. A low dose implant of 17β-estradiol prevented this OVX effect and reinstated apomorphine-induced PPI disruption. Following adolescent OVX, the effect of apomorphine was not altered and it significantly reduced PPI in adulthood. A low dose implant of 17β-estradiol following adolescent OVX effect blocked apomorphine-induced PPI disruption in adulthood. Apomorphine had no effect on PPI in any of the mice treated with the high dose of 17β-estradiol or a combination of low-dose 17β-estradiol and progesterone, irrespective of treatment age, suggesting an antipsychotic action. Apomorphine tended to disrupt PPI in mice treated with progesterone only, irrespective of age of OVX. These results suggest that in adult mice, circulating 17β-estradiol and progesterone play an important role in dopaminergic regulation of PPI. This role may develop during adolescence as similar effects of OVX and ovarian hormones were not observed following interventions in 5-week old mice. Our results also confirm and extend previous evidence that 17β-estradiol may have antipsychotic properties.

Anxiety is among the most prevalent mental health issues in children. While it is well established that gonadal steroids influence anxiety-like behavior in adulthood, a potential role in prepubertal juveniles has been overlooked because it is commonly thought that the gonads are quiescent during the juvenile period. However, the juvenile gonads secrete measurable amounts of steroids, and we have recently found that prepubertal ovariectomy decreases anxiety-like behavior of juvenile Siberian hamsters in the light/dark box test. The present study tested whether an injection of estradiol benzoate (1 μg or 10 μg, SC) to gonadectomized hamsters (Exp. 1) or chronic suppression of endogenous estradiol with the aromatase inhibitor, letrozole (2 mg/kg, PO), to intact hamsters (Exp. 2) affects anxiety-like behavior in the light/dark box test during the juvenile phase. Estradiol benzoate altered anxiety-like behavior of both male and female juveniles in a dose-dependent manner, with anxiolytic actions at the low dose, but no effect at the high dose. Similar effects were seen for activity measures, albeit only in females. Letrozole suppressed uterine weights demonstrating an active role for endogenous estradiol during the juvenile phase. Anxiety-like behavior, however, was impacted by the administration procedure itself, preventing conclusions on letrozole's actions on behavior. While the role for endogenous estradiol in juvenile anxiety-like behavior remains unresolved, the present findings indicate that the neural centers regulating affective behavior are responsive to exogenous estradiol prior to puberty. These findings highlight the potential impact of exogenous estrogen exposures on juvenile affective behavior.