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1.
Prolonged restriction of dietary energy delays onset of puberty, disrupts cyclicity in sexually mature animals, and lengthens the postpartum anestrous period in domestic ruminants. One important mechanism by which energy restriction impairs reproductive activity seems to be suppression of the increase in LH pulse frequency that is necessary for growth of ovarian follicles to the preovulatory stage. Under-nutrition apparently inhibits pulsatile secretion of LH by reducing LHRH secretion by the hypothalamus. The ability of an animal to sustain a high-frequency mode of pulsatile LH release is related to its metabolic status. Mechanisms linking metabolic status to LHRH secretion have not been fully characterized. Changes in body fat have been associated with changes in reproductive activity, but it is unlikely that body fat per se regulates LHRH secretion. It is possible that pulsatile LHRH release is regulated by specific metabolites and(or) metabolic hormones that reflect nutritional status. Alternatively, availability of oxidizable metabolic fuels, such as glucose and nonesterified fatty acids, may influence activity of neurons that control LHRH release. Our understanding of how the central nervous system transduces information about nutritional status into neuroendocrine signals that control reproduction in cattle and sheep is limited by a lack of information concerning the nature of neurons controlling LHRH release in these species.  相似文献   

2.
 人类的性早熟表现为病理状态,而在动物上,性早熟则是一个在生产上具有重要价值的经济性状。动物性成熟启动是一个复杂的生物学过程,受下丘脑-垂体-性腺轴调控。"允许信号"和"发育时钟"传达了机体生长发育、能量平衡和环境变化信息,决定了性成熟启动前期处于休眠状态的GnRH神经元激活;GnRH神经元抑制性输入减少和兴奋性输入增加引发了高频GnRH脉冲分泌,促进配子形成和性类固醇激素分泌;类固醇激素又通过负反馈通路影响GnRH分泌并促进性行为。神经胶质细胞也参与了性成熟的启动,主要涉及生长因子家族、神经细胞粘合分子和神经接触蛋白。GnRH基因的表观遗传修饰变化可能在动物性成熟启动过程中发挥了重要作用。  相似文献   

3.
Gonadotropin secretion by the pituitary gland is under the control of luteinizing hormone-releasing hormone (LHRH) and the putative follicle stimulating hormone-releasing factor (FSHRF). Lamprey III LHRH is a potent FSHRF in the rat and seems to be resident in the FSH controlling area of the rat hypothalamus. It is an analog of mammalian LHRH and may be the long sought FSHRF. Gonadal steroids feedback at hypothalamic and pituitary levels to either inhibit or stimulate the release of LH and FSH, which is also affected by inhibin and activin secreted by the gonads. Important control is exercised by acetylcholine, norepinephrine (NE), dopamine, serotonin, melatonin, and glutamic acid (GA). Furthermore, LH and FSH also act at the hypothalamic level to alter secretion of gonadotropins. More recently, growth factors have been shown to have an important role. Many peptides act to inhibit or increase release of LH and the sign of their action is often reversed by estrogen. A number of cytokines act at the hypothalamic level to suppress acutely the release of LH but not FSH. NE, GA, and oxytocin stimulate LHRH release by activation of neural nitric oxide synthase (nNOS). The pathway is as follows: oxytocin and/ or GA activate NE neurons in the medial basal hypothalamus (MBH) that activate NOergic neurons by alpha1 (α1) receptors. The NO released diffuses into LHRH terminals and induces LHRH release by activation of guanylate cyclase (GC) and cyclooxygenase. NO not only controls release of LHRH bound for the pituitary, but also that which induces mating by actions in the brain stem. An exciting recent development has been the discovery of the adipocyte hormone, leptin, a cytokine related to tumor necrosis factor (TNF) α. In the male rat, leptin exhibits a high potency to stimulate FSH and LH release from hemipituitaries incubated in vitro, and increases the release of LHRH from MBH explants. LHRH and leptin release LH by activation of NOS in the gonadotropes. The NO released activates GC that releases cyclic GMP, which induces LH release. Leptin induces LH release in conscious, ovariectomized estrogen-primed female rats, presumably by stimulating LHRH release. At the effective dose of estrogen to activate LH release, FSH release is inhibited. Leptin may play an important role in induction of puberty and control of LHRH release in the adult as well.  相似文献   

4.
The inhibitory effect of inflammation and endotoxins on the secretion of reproductive hormones from the hypothalamo-pituitary axis is well documented. A comparison of the luteinizing hormone (LH) suppressing effects of several pro-inflammatory cytokines revealed that centrally administered IL-1β was the most potent inhibitor of pituitary LH secretion; interleukin (IL)-1α and tumor necrosis factor (TNF)α were relatively less effective, whereas IL-6 was ineffective. This order of potency suggested that the anti-gonadotropic effects of an immune challenge are most likely attributable to the action of centrally released IL-1β, and this was supported by the demonstration that IL-1β suppressed hypothalamic luteinizing hormone releasing hormone (LHRH) release. We used a multifaceted approach to identify the afferent signals in the brain that convey immune messages to hypothalamic LHRH neurons. Pharmacological studies with specific antagonists of opioid receptor subtypes demonstrated that activation of the μ1 receptor subtype was required to transmit the cytokine signal. Furthermore, icv IL-1β upregulated hypothalamic POMC mRNA and increased the concentration and release of β-endorphin, the primary ligand of μ1 receptors. We have obtained evidence that IL-1β also enhanced the gene expression and concentration of tachykinins, a family of nociceptive neuropeptides in the hypothalamus. Blockade of tachykinergic NK2 receptors attenuated IL-1β induced inhibition of LH secretion. Collectively, these results demonstrate that IL-1β, generated centrally in response to inflammation, upregulates the opioid and tachykinin peptides in the hypothalamus. These two groups of neuropeptides are critically involved in relaying the cytokine signal to neuroendocrine neurons and causing the suppression of hypothalamic LHRH and pituitary LH release.  相似文献   

5.
Bidirectional communication between the neuroendocrine and immune systems plays a pivotal role in health and disease. Signals generated by the hypothalamic-pituitary-gonadal (HPG) axis (i.e. luteinizing hormone-releasing hormone, LHRH, and sex steroids) are major players coordinating the development immune system function. Conversely, products generated by immune system activation exert powerful and longlasting effects on HPG axis activity. In the central nervous system (CNS), one chief neuroendocrine-immune (NEI) compartment is represented by the astroglial cell population and its mediators. Of special interest, the major supporting cells of the brain and the thymus, astrocytes and thymic epithelial cells, share a similar origin and a similar set of peptides, transmitters, hormones and cytokines functioning as paracrine/autocrine regulators. This may explain some fundamental analogies in LHRH regulation of both cell types during ontogeny and in adult life. Hence, the neuropeptide LHRH significantly modulates astrocyte and thymic cell development and function. Here we focus this work on LHRH neuron-glial signaling cascades which dictate major changes during LHRH neuronal differentiation and growth as well as in response to hormonal manipulations and pro-inflammatory challenges. The interplay between LHRH, growth factors, estrogens and pro-inflammatory mediators will be discussed, and the potential physiopathological implications of these findings summarized. The overall study highlights the plasticity of this intersystem cross-talk and emphasize neuron-glial interactions as a key regulatory level of neuroendocrine axes activity.  相似文献   

6.
There has been extensive research of the anterior pituitary gland of livestock and poultry due to the economic (agricultural) importance of physiological processes controlled by it including reproduction, growth, lactation and stress. Moreover, farm animals can be biomedical models or useful in evolutionary/ecological research. There are for multiple sites of control of the secretion of anterior pituitary hormones. These include the potential for independent control of proliferation, differentiation, de-differentiation and/or inter-conversion cell death, expression and translation, post-translational modification (potentially generating multiple isoforms with potentially different biological activities), release with or without a specific binding protein and intra-cellular catabolism (proteolysis) of pituitary hormones. Multiple hypothalamic hypophysiotropic peptides (which may also be produced peripherally, e.g. ghrelin) influence the secretion of the anterior pituitary hormones. There is also feedback for hormones from the target endocrine glands. These control mechanisms show broadly a consistency across species and life stages; however, there are some marked differences. Examples from growth hormone, prolactin, follicle stimulating hormone and luteinizing hormone will be considered. In addition, attention will be focused on areas that have been neglected including the role of stellate cells, multiple sub-types of the major adenohypophyseal cells, functional zonation within the anterior pituitary and the role of multiple secretagogues for single hormones.  相似文献   

7.
It has been well recognized that interactions between the gut microbiota and host-metabolism have a proven effect on health. The gut lumen is known for harboring different bacterial communities. Microbial by-products and structural components, which are derived through the gut microbiota, generate a signaling response to maintain homeostasis. Gut microbiota is not only involved in metabolic disorders, but also participates in the regulation of reproductive hormonal function. Bacterial phyla, which are localized in the gut, allow for the metabolization of steroid hormones through the stimulation of different enzymes. Reproductive hormones such as progesterone, estrogen and testosterone play a pivotal role in the successful completion of reproductive events. Disruption in this mechanism may lead to reproductive disorders. Environmental bacteria can affect the metabolism, and degrade steroid hormones and their relevant compounds. This behavior of the bacteria can safely be implemented to eliminate steroidal compounds from a polluted environment. In this review, we summarize the metabolism of steroid hormones on the regulation of gut microbiota and vice-versa, and also examined the significant influence this process has on various events of reproductive function. Altogether, the evidence suggests that steroid hormones and gut microbiota exert a central role in the modification of host bacterial action and impact the reproductive efficiency of animals and humans.  相似文献   

8.
The goal of this study was to evaluate the effect of various concentrations of interferon-tau (IFN-tau) with or without steroid hormones, 171 estradiol or progesterone, on the proliferation of bovine endometrial cells in vitro. Endometrial epithelial and stromal cells were isolated from the uterus of cows during the early estrus cycle (2-3 days) and incubated with different doses of IFN-tau with or without steroid hormones. The proliferation was determined by the MTT test in 48, 96, and 144 h of incubation. An antiproliferative activity of IFN-tau was observed both in epithelial and stromal cells cultured in RPMI 1640 medium supplemented with 10% FBS or. serum replacement. However, epithelial cells were more sensitive to antiproliferative action of interferon-tau. It;s activity was dose-and time-dependent. The inhibition of epithelial cell proliferation by 50% (ED50) was achieved at concentrations of 500 U/ml, 340 U/ml, and 8.8 U/ml of IFN-tau after 48, 96, and 144 h of incubation, respectively. None of the doses of IFN-tau (10-10.000 U/ml) used inhibited stromal cell proliferation in 50%. The most effective dose of IFN-tau inhibiting stromal cell proliferation was 10.000 U/ml, which decreased cell growth by 17.08%, 22.87%, and 2.6% after 48, 96, and 144 h of incubation, respectively. Steroid hormones, 17beta estradiol and progesterone, added to the culture of stromal cells with or without IFN-tau did not significantly modulate stromal cell growth. In contrast, a high concentration of progesterone (10(-5) M) alone significantly enhanced stromal cell growth. Progesterone at low, physiological concentrations (10(-7)- 10(-9) M) ameliorated the antiproliferative activity of IFN-tau, especially at the 10(-9 )M concentration. At this concentration, the stimulatory effect on stromal cell growth was observed. The mechanisms of such response are not entirely clear but may arise from the influence of IFN-tau on progesterone down regulation of its own receptor. Depicted activity of IFN-tau may find usefulness in therapy of neoplastic disorders.  相似文献   

9.
Steroid hormones have a profound influence on the secretion of the gonadotropins, follicle-stimulating hormone (FSH) and luteinizing hormone (LH). These effects can occur as a result of steroid hormones modifying the secretion of gonadotropin-releasing hormone (GnRH) from the hypothalamus, or a direct effect of steroid hormones on gonadotropin secreting cells in the anterior pituitary gland. With respect to the latter, we have shown that estradiol increases pituitary sensitivity to GnRH by stimulating an increase in expression of the gene encoding the GnRH receptor. Since an estrogen response element (ERE) has not been identified in the GnRH receptor gene, this effect appears to be mediated by estradiol stimulating production of a yet to be identified factor that in turn enhances expression of the GnRH receptor gene. However, the importance of estradiol for enhancing pituitary sensitivity to GnRH during the periovulatory period is questioned because an increase in mRNA for the GnRH receptor precedes the pre-ovulatory rise in circulating concentrations of estradiol. In fact, it appears that the enhanced pituitary sensitivity during the periovulatory period may occur as a result of a decrease in concentrations of progesterone rather than due to an increase in concentrations of estradiol. Estradiol also is capable of altering secretion of FSH and LH in the absence of GnRH. In a recent study utilizing cultured pituitary cells from anestrous ewes, we demonstrated that estradiol induced a dose-dependent increase in secretion of LH, but resulted in a dose-dependent decrease in the secretion of FSH. We hypothesized that the discordant effects on secretion of LH and FSH might arise from estradiol altering the production of some of the intrapituitary factors involved in synthesis and secretion of FSH. To examine this hypothesis, we measured amounts of mRNA for activin B (a factor known to stimulate synthesis of FSH) and follistatin (an activin-binding protein). We found no change in the mRNA for follistatin after treatment of pituitary cells with estradiol, but noted a decrease in the amount of mRNA for activin B. Thus, the inhibitory effect of estradiol on secretion of FSH appears to be mediated by its ability to suppress the expression of the gene encoding activin.  相似文献   

10.
Several different amino acids and peptides control secretion of adenohypophysial hormones and this control may be indirect, via the modulation of hypothalamic hormone secretion. Indeed, classical hypothalamic hormones (e.g., gonadotropin-releasing hormone [GnRH], growth hormone-releasing hormone [GHRH], somatostatin, etc.) may be released into the hypothalamo-hypophysial portal vasculature, travel to the adenohypophysis and there stimulate or inhibit secretion of hormones. Alternatively, some amino acids and peptides exert direct stimulatory or inhibitory effects on the adenohypophysis, thereby impacting hormone secretion. In swine, the most extensively studied modulators of adenohypophysial hormone secretion are the excitatory amino acids (ExAA), namely glutamate and aspartate, and the endogenous opioid peptides (EOP). In general, excitatory amino acids stimulate release of luteinizing hormone (LH), follicle-stimulating hormone (FSH), growth hormone (GH), and prolactin (PRL). Secretion of adenohypophysial hormones induced by ExAA is primarily, but perhaps not exclusively, a consequence of action at the central nervous system. By acting primarily at the level of the central nervous system, EOP inhibit LH secretion, stimulate GH release and depending on the animal model studied, exert either stimulatory or inhibitory influences on PRL secretion. However, the EOP also inhibited LH release by direct action on the adenohypophysis. More recently, peptides such as neuropeptide-Y (NPY), orexin-B, ghrelin, galanin, and substance P have been evaluated for possible roles in controlling adenohypophysial hormone secretion in swine. For example, NPY, orexin-B, and ghrelin increased basal GH secretion and modulated the GH response to GHRH, at least in part, by direct action on the adenohypophysis. Secretion of LH was stimulated by orexin-B, galanin, and substance P from porcine pituitary cells in vitro. Because the ExAA and various peptides modulate secretion of adenohypophysial hormones, these compounds may play an important role in regulating swine growth and reproduction.  相似文献   

11.
The direct effects of three steroid hormones (progesterone, estradiol-17beta and corticosterone) on the growth of Neospora caninum (N. caninum) tachyzoite were examined in Vero cells. Subsequently, ovariectomized BALB/c mice infected with N. caninum were treated with physiological concentrations of the steroid hormones for 1 or 2 weeks. These hormones had no direct effect on the parasite growth in vitro. In the infected mice, there was no significant difference in the parasite distribution and histopathological changes between the hormone-injected and control groups. No mice showed parasitemia at the time of autopsy. These results suggest that physiological levels of steroid hormones (progesterone, estradiol-17beta and corticosterone) do not reactivate N. caninum in mice.  相似文献   

12.
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13.
动物体内的许多激素和因子通过内分泌活动把能量摄入和繁殖系统联系起来。卵巢上卵泡的发育是雌性动物繁殖系统中的重要因素,是繁殖性能的基础。猪的生产是人们生活中主要的肉类来源之一,能量对猪卵泡发育的影响日益受到关注。日粮能量水平的变化会影响到体内循环与营养代谢相关的激素和因子,而这些激素和因子的变化可能会作为代谢信号对卵泡的发育产生影响。这些代谢信号包括胰岛素、瘦素和胰岛素样生长因子-Ⅰ等。研究表明,代谢信号对下丘脑、垂体和卵巢均有影响。在胰岛素、瘦素和胰岛素样生长因子-Ⅰ等代谢信号的介导下,日粮能量营养因素通过改变下丘脑-垂体-卵巢轴的活性,对雌性动物的卵泡发育产生影响。  相似文献   

14.
In relevance to osmoregulatory and reproductive functions, activity of hypothalamic neurosecretory neurons may also vary seasonally. The current study was performed to determine annual changes in ir-AVT neurons of hypothalamus and adrenal gland function. We examined changes in ir-AVT neuron by immunohistochemical method and plasma testosterone was measured by enzyme immunoassay. The steroidogenic interrenal activity was studied by histological and biochemical methods. Birds were sampled in February (quiescent), April (recrudescent), June (breeding) and November (regressive). A significant and gradual increase in the number of ir-AVT neurons was observed from quiescent to breeding phase which decreased during regressive phase of annual gonadal cycle. The gradual increase in ir-AVT neurons along with annual gonadal activity of quail were accompanied by increase in plasma levels of testosterone. These results indicate a functional interaction between sex steroid and AVT synthesizing neurons. Adrenal activity (as judged by weight, ascorbic acid content, cortical cord width and cortico-medullary ratio) was also maximum during breeding phase. It is thus postulated that domesticated quail when exposed to natural day length (NDL), exhibits seasonal/annual cyclicity in vastocinergic activity and adrenal function which may be due to difference in sex steroid hormone.  相似文献   

15.
The need for accurate selection of the best oocytes for in vitro fertilization protocols and thus, production of embryos has driven the search for oocyte quality markers from morphological criteria to biochemical parameters. Current studies are focused on the biochemical constituents of the follicular fluid and gene expression profiling of the cumulus cells. These parameters are, however, affected by factors that must be considered before making a judgment of the oocyte's quality. These includes factors such as the type of hormonal stimulation protocol, age of oocyte donor and heat stress on the donor, all of which have been reported to influence the concentrations of many hormones, apolipoproteins, metabolites, fatty acids and growth factors in the follicular fluid and the expression of several genes in the cumulus cells. Another important point to note is species variation in the response to these extraneous influences, which thus calls for species targeted investigations. As reports are still scanty and investigations assumed to be very keen, we employed this review paper to bring attention of researchers and clinicians to those factors that may come to bear on the outcome of their investigations on oocyte and embryo quality.  相似文献   

16.
Olfactory glial cells have been the focus of much recent research interest because of their possible future use as cellular transplants in repair of spinal cord injury. Although olfactory glial cells can be collected from the olfactory bulb for in vitro culture, alternative sites would be preferable for safer surgical access. This study was designed to investigate the distribution of olfactory sensory neurons and olfactory glial cells within the canine peripheral olfactory system. Using immunohistochemistry and electron microscopy on perfused tissue we demonstrate that olfactory sensory neurons are found in both the caudal nasal and the frontal sinus epithelia. Olfactory ensheathing glia were found in the mucosa at both these sites implying that surgical access for harvesting cells for transplantation would be straightforward.  相似文献   

17.
运用免疫组织化学超敏 SP法对山羊胎儿脊髓发育中神经生长因子 (nerve growth factor,NGF)及其高亲和力受体 Tr KA的表达及其功能进行了系统的研究和探讨。结果显示 ,山羊胎儿脊髓灰质中存在 NGF及其受体 Tr KA,于 6周龄胚就可检测到 ,随胚龄增加 ,其表达范围及免疫反应着色程度逐渐增强。 NGF主要分布于腹角和背角的神经细胞 ,反应产物主要定位于胞质和突起 ;Tr KA的分布主要以腹角及胶状质为主 ,反应产物主要定位于胞核 ,后期胞质及突起也可见到阳性反应。在山羊胎儿脊髓白质中也可观察到 NGF及 Tr KA免疫阳性反应 ,其发育后期更为显著 ,阳性反应主要分布于神经胶质细胞核、神经纤维的轴索及雪旺氏细胞。结果提示 ,NGF不仅对交感和感觉神经元的发育起作用 ,而且还与腹角运动神经元的发育有关  相似文献   

18.
The mammalian ovary is an extremely dynamic organ in which a large majority of follicles are effectively eliminated throughout their reproductive life. Due to the numerous efforts of researchers, mechanisms regulating follicular growth and atresia in mammalian ovaries have been clarified, not only their systemic regulation by hormones (gonadotropins) but also their intraovarian regulation by gonadal steroids, growth factors, cytokines and intracellular proteins. Granulosa cells in particular have been demonstrated to play a major role in deciding the fate of follicles, serving molecules that are essential for follicular growth and maintenance as well as killing themselves by an apoptotic process that results in follicular atresia. In this review, we discuss the factors that govern follicular growth and atresia, with a special focus on their regulation by granulosa cells. First, ovarian folliculogenesis in adult life is outlined. Then, we explain about the regulation of follicular growth and atresia by granulosa cells, in which hormones, growth factors and cytokines, death ligand-receptor system and B cell lymphoma/leukemia 2 (BCL2) family members (mitochondria-mediated apoptosis) are further discussed.  相似文献   

19.
Our understanding of the development and progression of equine pituitary pars intermedia (PI) dysfunction has expanded over the last decade, although much remains to be explained. Degeneration of the hypothalamic periventricular dopaminergic neurons results in disinhibition of the endocrine cells of the PI, the melanotropes. As a result, the PI enlarges, compressing the adjacent lobes, the pars distalis and pars nervosa. The disinhibited melanotropes overproduce pro‐opiomelanocortin peptides, including α‐melanocyte stimulating hormone, β‐endorphin, corticotrophin‐like intermediate lobe peptide and adrenocorticotropin. The excess in PI hormones, perhaps in concert with a deficiency in other pituitary hormones, results in clinical signs of pituitary PI dysfunction. Evidence suggests both oxidative stress and accumulation of misfolded neuronal proteins contribute to damage to the periventricular neurons, although it is not clear if these pathologies actually initiate the disease or are downstream events.  相似文献   

20.
Oestrogen (E2) and thyroid hormones (THs) are key regulators of cerebellar development. Recent reports implicate a complex mechanism through which E2 and THs influence the expression levels of each other's receptors (ERs and TRs) to precisely mediate developmental signals and modulate signal strength. We examined the modulating effects of E2 and THs on the expression levels of their receptor mRNAs and proteins in cultured cerebellar cells obtained from 7-day-old rat pups. Cerebellar granule cell cultures were treated with either E2, THs or a combination of these hormones, and resulting receptor expression levels were determined by quantitative PCR and Western blot techniques. The results were compared to non-treated controls and to samples obtained from 14-day-old in situ cerebella. Additionally, we determined the glial effects on the regulation of ER-TR expression levels. The results show that (i) ER and TR expression depends on the combined presence of E2 and THs; (ii) glial cells mediate the hormonal regulation of neuronal ER-TR expression and (iii) loss of tissue integrity results in characteristic changes in ER-TR expression levels. These observations suggest that both E2 and THs, in adequate amounts, are required for the precise orchestration of cerebellar development and that alterations in the ratio of E2/THs may influence signalling mechanisms involved in neurodevelopment. Comparison of data from in vitro and in situ samples revealed a shift in receptor expression levels after loss of tissue integrity, suggesting that such adjusting/regenerative mechanisms may function after cerebellar tissue injury as well.  相似文献   

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