The role of photoperiod and melatonin in the control of seasonal reproduction in mammals

<b>Melatonin secreted by pineal cells is a hormone whose biosynthesis is coordinated by neurons of the master clock located in the hypothalamic suprachiasmatic nuclei (SCN), characterized by the generation of a 24-hour rhythm. In many species of mammals, fluctuations in melatonin secretion affect reproductive functions, e.g. by regulating the frequency and amount of pulsatile secretion of hypothalamic and gonadotropic hormones. Seasonal breeding is a common adaptive strategy among mammals, allowing them to reproduce during the periods of the year that are most favourable for the later survival and growth of the offspring. This type of reproduction is characteristic of sheep, with winter reproductive activity, and hamsters, with summer reproductive activity. In these animals, melatonin synthesis is largely regulated by the photoperiod, which indirectly influences the period of reproductive activity or passivity. The aim of this study was to gather available knowledge on melatonin as a key element controlling seasonal reproduction. The paper presents the general shape of the circadian rhythm and the neuroendocrine mechanism regulating animal reproduction depending on the variable photoperiod. The collected results suggest that melatonin, kisspeptins, gonadotropin-releasing hormone (GnRH), sex hormones and thyroid hormones participate in the regulation of seasonal reproduction in mammals. </b>

Oxytocin-like signal regulates Lh cells directly but not Fsh cells in the ricefield eel Monopterus albus†

The synthesis and release of LH and FSH in the pituitary of vertebrates are differentially regulated during gonadal development and maturation. However, the underlying neuroendocrine mechanisms remain to be fully elucidated. The present study examined the possible involvement of isotocin (Ist), an oxytocin-like neuropeptide, in the regulation of Lh and Fsh in a teleost, the ricefield eel Monopterus albus. The immunoreactive isotocin receptor 2 (Istr2) was shown to be localized to Lh but not Fsh cells. In contrast, immunoreactive isotocin receptor 1 (Istr1) was not observed in either Lh or Fsh cells in the pituitary. Interestingly, Lh cells in female ricefield eels expressed Istr2 and secreted Lh in response to Ist challenge stage-dependently and in correlation with ovarian vitellogenesis. Moreover, Ist decreased Lh contents in the pituitary of female fish, indicating its stimulatory roles on Lh release in vivo. The induction of Lh release by Ist in dispersed pituitary cells was blocked by a PLC or IP3R inhibitor but not by a PKA or PKC inhibitor, indicating the involvement of the IP3/Ca2+ pathway. Collectively, the above results indicate that isotocin may bind to Istr2 to stimulate Lh release via the IP3/Ca2+ pathway, and play important roles in the ovarian maturation in ricefield eels. Furthermore, the present study suggests a novel neuroendocrine mechanism underlying the differential regulation of Lh and Fsh in vertebrates.

Study on the Pathogenesis of Poststroke Depression

The main pathogenesis of post-stroke depression (PSD) can be divided into five aspects, that is the neuroanatomical mechanism, neurotransmitter mechanism, neuroendocrine mechanism, inflammatory factor mechanism and the target gene mechanism of depression-related possible effects regulated by miR30a-5p. Post-stroke depression acts on stroke patients through the above five mechanisms, bringing pain to patients and their families.In order to better solve such problems, it is necessary to clarify its pathogenesis in detail. This article mainly reviews the research content, clinical treatment and prospects of the pathogenesis of post-stroke depression.

Octopamine and cooperation: octopamine regulates the disappearance of cooperative behaviours between genetically unrelated founding queens in the ant

We investigated whether octopamine (OA) is associated with the disappearance of cooperation in Polyrhachis moesta ant queens. Queens of P. moesta facultatively found the colony with genetically unrelated queens. The founding queens perform frequent food exchange with these non-related queens and partake in cooperative brood rearing, whereas single colony queens exclude non-related queens via aggressive behaviour. Thus, aggression is a factor that reduces cooperation. Given that aggression is generally associated with brain OA in insects, we hypothesized that OA controls the behavioural change in cooperation in the ant queen, via an increase in aggression. To test this hypothesis, we compared the amounts of OA and related substances in the brain between founding and colony queens, and observed the interaction of founding queens following oral OA administration. The brain OA levels in colony queens were significantly higher than those in founding queens. Oral administration of OA to founding queens caused significantly less trophallaxis and allogrooming behaviour than in the control founding queens, but with no significant increase in aggression. These results suggest that OA promotes the disappearance of cooperation in founding queens of P. moesta . This is the first study to reveal the neuroendocrine mechanism of cooperation in ant queens.

Testosterone biases the amygdala toward social threat approach

Testosterone enhances amygdala reactions to social threat, but it remains unclear whether this neuroendocrine mechanism is relevant for understanding its dominance-enhancing properties; namely, whether testosterone biases the human amygdala toward threat approach. This pharmacological functional magnetic-resonance imaging study shows that testosterone administration increases amygdala responses in healthy women during threat approach and decreases it during threat avoidance. These findings support and extend motivational salience models by offering a neuroendocrine mechanism of motivation-specific amygdala tuning.

Effects of systemic administration or intrabursal injection of serotonin on puberty, first ovulation and follicular development in rats

To elucidate the role of serotonin in the onset of puberty, the effects of both systemic and in-ovarian bursa administration of serotonin on the neuroendocrine mechanism that modulates the onset of puberty, follicular development and first ovulation were evaluated. Two experiments were carried out. For the first, 25 or 37.5 mg kg–1 of bodyweight of serotonin creatinine sulfate was administered by a subcutaneous route to 30-day-old female rats. In the second experiment, serotonin creatinine sulfate was administered directly into the ovarian bursa of 34-day-old female rats. Systemic administration of 25 or 37.5 mg kg–1 of serotonin creatinine sulfate induced a delay in the ages of vaginal opening and first vaginal oestrus, a decrease in the number of ovulating animals, and serum concentrations of FSH, LH, oestradiol and progesterone. An increase in the number of Class 3 (>500 μm) and atretic follicles was observed in the ovaries of these animals. The administration of serotonin creatinine sulfate in the ovarian bursa did not modify the onset of puberty and ovulation, but a reduced serum concentration of oestradiol was observed. Our results suggest that serotonin acts on the components of the hypothalamus–hypophysis–ovary axis by modulating follicular development, ovarian functions and the onset of puberty.