The changes in distribution and concentration of neuropeptides, gonadotropin-releasing hormone (GnRH), gonadotropin-inhibitory hormone (GnIH), kisspeptin, and gonadotropin-releasing hormone receptor (GnRH-R) were evaluated and compared with reproductive parameters, such as cytochrome P450 side-chain cleavage (P450 SCC) enzyme activity, androgen receptors (AR) in the testis and serum testosterone levels, from birth to senescence in mice. The results showed the localization of these molecules mainly in the interstitial and germ cells as well as showed significant variations in immunostatining from birth to senescence. It was found that increased staining of testicular GnRH-R coincided with increased steroidogenic activity during pubertal and adult stages, whereas decreased staining coincides with decreased steroidogenic activity during senescence. Similar changes in immunostaining were confirmed by Western/slot blot analysis. Thus, these results suggest a putative role of GnRH during testicular pubertal development and senescence. Treatment with a GnRH agonist ([DTrp6, Pro9-NEt] GnRH) to mice from prepubertal to pubertal period showed a significant increase in steroidogenic activity of the mouse testis and provided further support to the role of GnRH in testicular pubertal maturation. The significant decline in GnRH-R during senescence may be due to a significant increase in GnIH synthesis during senescence causing the decrease in GnRH-R expression. It is considered that significant changes in the levels of GnRH-R may be responsible for changes in steroidogenesis that causes either pubertal activation or senescence in testis of mice. Furthermore, changes in the levels of GnRH-R may be modulated by interactions among GnRH, GnIH, and kisspeptin in the testis.

Gonadotropin releasing hormone (GnRH) has now been suggested as an important intraovarian regulatory factor. Gonadotropin inhibitory hormone (GnIH) a hypothalamic dodecapeptide, acts opposite to GnRH. GnRH, GnIH and their receptors have been demonstrated in the gonads. In order to find out the physiological significance of these neuropeptides in the ovary, we aim to investigate changes in the abundance of GnRH I and GnIH in the ovary of mice during estrous cycle. The present study investigated the changes in GnRH I, GnRH I-receptor and RFRP-3 protein expression in the ovary of mice during estrous cycle by immunohistochemistry and immunoblot analysis. The immunoreactivity of GnRH I and its receptor and RFRP-3 were mainly localized in the granulosa cells of the healthy and antral follicles during proestrus and estrus and in the luteal cells during diestrus 1 and 2 phases. The relative abundance of immunoreactivity of GnRH I, GnRH I-receptor and RFRP-3 undergo significant variation during proestrus and thus may be responsible for selection of follicle for growth and atresia. A significant increase in the concentration of RFRP-3 during late diestrus 2 coincided with the decline in corpus luteum activity and initiation of follicular growth and selection. In general, immunolocalization of GnRH I, GnRH I-receptor and RFRP-3 were found in close vicinity suggesting functional interaction between these peptides. It is thus, hypothesized that interaction between GnRH I-RFRP-3 neuropeptides may be involved in the regulation of follicular development and atresia.

Tumor necrosis factor alpha (TNF alpha) has previously been immunolocalized within mouse oocytes. Our first objective was to examine TNF alpha immunolocalization in ovaries of adult, fetal, and neonatal rats. Our second objective was to examine TNF alpha mRNA in ovaries by Northern blot analysis and in oocytes by reverse-transcriptase polymerase chain reaction (RT-PCR). Our final objective was to determine whether oocytes contained bioactive TNF alpha. Ovaries and oviducts were collected throughout the estrous cycle in adult rats, fetal ovaries were obtained 1 day before expected delivery, and neonatal ovaries were collected 2 days after birth. TNF alpha was localized in tissues by a biotin-avidin immunocytochemical procedure. Immunocytochemistry in adult ovaries showed that the ooplasm of the oocyte was the primary site of TNF alpha localization within the follicle. Immunostaining was present in all oocytes in the adult, including ovulated oocytes within the oviduct. Oocytic TNF alpha immunostaining was also present within oocytes in the neonate; however, fetal oocytes did not contain immunoreactive TNF alpha. Northern blots showed that ovaries in the adult, neonate, and fetus all contained TNF alpha mRNA. RT-PCR analysis of oocytes collected from preovulatory follicles generated a cDNA band of 500 bp, corresponding to the predicted size for amplified TNF alpha cDNA. Subsequent Southern blot analysis showed that the 500-bp band hybridized to the TNF alpha probe, indicating that preovulatory oocytes contain TNF alpha mRNA. Preovulatory oocytes were used in TNF alpha cytotoxicity assays with L929 cells. Oocytes contained TNF alpha bioactivity that was similar to that of recombinant murine TNF alpha in the bioassay. Our results provide evidence for the identification of immunoreactive and bioactive TNF alpha within oocytes in the rat, which is further supported by the presence of TNF alpha mRNA within the oocyte. These studies also indicate that TNF alpha may appear in the oocyte around the time of birth.

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The findings of this study thus suggest that bhang may impair fertility in male mice through alteration in the testicular endocannabinoid system and that chronic bhang exposure in humans would be predicted to alter male fertility.

Metabolic disorders such as obesity and type 2 diabetes are one of the most familiar risk factors in the present time among every age-group. It is associated with altered levels of adipokines such as adiponectin, chemerin, leptin, resistin, visfatin, and so on. Adiponectin is one of the adipocyte-specific protein with novel applications pertaining to metabolism by promoting insulin sensitivity and regulating glucose and fatty acid catabolism, while chemerin is considered as an inhibitor of insulin signaling and glucose catabolism. Other than these established functions, both the adipokines are intimately involved in coordinating reproductive activities, but they exhibit contrary functions. This review is an amalgamation of recent information related to adiponectin and chemerin in male and female reproduction and further its association with metabolism-related reproductive disorders. The direct effect of adiponectin and chemerin on various reproductive parameters has been investigated, but there was a rampant failure to account for in vivo data which gives a broad outlook on the regulatory mechanism of both adiponectin and chemerin related to male and female reproductive functions. Adiponectin is known to promote gonadal activities, while chemerin exerts antigonadal actions. Recent research suggests that high chemerin/low adiponectin ratio plays a vital role in causing dyslipidemia and metabolic syndrome in patients. The dysregulated ratio of adiponectin to chemerin during various metabolic disorders makes it really worthy in relation to an application for therapeutics. Still, a lot regarding both the adipokines has to be explored and brought forward in order to deal with therapeutics of metabolism-related reproductive disorders.

The aim of the study was to evaluate the seasonal variation in serum leptin levels in a natural population of the female bat, Scotophilus heathi and their relationship to the changes in the body mass, serum insulin level, and ovarian activity. Circulating leptin level varied significantly over the season and correlated positively with the changes in body mass, and circulating insulin and androstenedione (A4) levels. Circulating leptin concentrations showed two peaks; one coincides with the maximum fat accumulation prior to winter dormancy, whereas the second shorter peak coincides with late pregnancy. The in vivo study in S. heathi showed that the increased circulating leptin level during winter dormancy coincides with the decreased expression of ovarian steroidogenic acute regulatory (StAR) protein, and low circulating estradiol (E 2 ) level. At the same time, increased circulating leptin level coincides with increased expression of ovarian insulin receptor and high circulating A4 level. The low circulating leptin level during preovulatory period coincides with the increase in StAR protein but decrease in insulin receptor protein. The in vitro study confirmed the in vivo observations of inhibitory effect of leptin on LH induced StAR expression and E 2 production, whereas the stimulatory effect of leptin (high dose) on LH induced expression of insulin receptor protein and A4 production. However, pharmacological dose of leptin produced inhibitory effect on the expression of insulin receptor protein.The results of the present study thus suggest that high circulating leptin level during winter dormancy promotes adiposity and impairs ovarian activity by suppressing StAR-mediated E 2 production as well as by enhancing insulin receptor-mediated A4 synthesis thereby contributing anovulatory condition of delayed ovulation in S. heathi.

Mast cells, endothelial cells, basophils and platelets are potential sources of histamine in the ovary. Little is known about the role of the latter three cell types in ovarian function. Several studies have revealed changes in the number and degranulation (release of histamine) of mast cells in the ovary during the cycle. Mast cells degranulate on pro-oestrus in the rodent ovary, and mast cells numbers increase in the theca externa of the dominant follicle in the bovine ovary. In rodents, mast cells are limited to the ovarian hilum and are not observed in follicles, corpora lutea and interstitium; this contrasts with larger species such as man, cows and monkeys where mast cells are observed throughout the ovary. Evidence is accumulating that mast cell degranulation in the ovary may be regulated by neuronal input. Neurones have been shown to have close morphological relationships with mast cells in the ovary. Histamine participates in regulating capillary permeability and blood flow in the ovary. These actions are induced by injections of LH, yet the mechanism by which LH induces mast cell degranulation is unknown. Histamine stimulates ovarian contractility, ovulation and follicular progesterone secretion in vitro. Whether these actions of histamine occur in vivo are currently unknown. This review gives a chronological description of the discoveries of the effects of histamine on ovarian function and makes suggestions for future research in this area.