[OA] Rudolph LM, Bentley GE, Calandra RS, et al. Peripheral and central mechanisms involved in hormonal control of male and female reproduction. J Neuroendocrinol. Peripheral and central mechanisms involved in hormonal control of male and female reproduction - Rudolph - Journal of Neuroendocrinology - Wiley Online Library
Reproduction involves the integration of hormonal signals acting across multiple systems to generate a synchronized physiological output. A critical component of reproduction is the luteinizing hormone (LH) surge, which is mediated by estradiol (E2) and neuroprogesterone interacting to stimulate kisspeptin release in the rostral periventricular nucleus of the third ventricle in rats. Recent evidence has shown that both classical and membrane E2 and progesterone signaling is involved in this pathway.
A metabolite of gonadotropin-releasing hormone (GnRH), GnRH-(1-5), has been shown to stimulate GnRH expression, secretion, and has a role in the regulation of lordosis. Additionally, gonadotropin-inhibitory hormone (GnIH) projects to and influences the activity of GnRH neurons in birds. Stress-induced changes in GnIH have been shown to alter breeding behaviors in birds, demonstrating another molecular control of reproduction.
Peripherally, paracrine and autocrine actions within the gonad have been suggested as therapeutic targets for infertility in both males and females. Dysfunction of testicular prostaglandin synthesis is a possible cause of idiopathic male infertility. Indeed, local production of melatonin and corticotropin-releasing hormone (CRH) could influence spermatogenesis via immune pathways in the gonad.
In females, vascular endothelial growth factor A (VEGF-A) has been implicated in an angiogenic process that mediates development of the corpus luteum and thus fertility via the Notch signaling pathway. Age-induced decreases in fertility involve ovarian kisspeptin and its regulation of ovarian sympathetic innervation.
Finally, morphological changes in the arcuate nucleus of the hypothalamus influence female sexual receptivity in rats. The processes mediating these morphological changes have been shown to involve rapid effects of E2 controlling synaptogenesis in this hypothalamic nucleus.
Together, this review highlights new research in these areas, focusing on recent findings in the molecular mechanisms of central and peripheral hormonal control of reproduction. This article is protected by copyright. All rights reserved.
Reproduction involves the integration of hormonal signals acting across multiple systems to generate a synchronized physiological output. A critical component of reproduction is the luteinizing hormone (LH) surge, which is mediated by estradiol (E2) and neuroprogesterone interacting to stimulate kisspeptin release in the rostral periventricular nucleus of the third ventricle in rats. Recent evidence has shown that both classical and membrane E2 and progesterone signaling is involved in this pathway.
A metabolite of gonadotropin-releasing hormone (GnRH), GnRH-(1-5), has been shown to stimulate GnRH expression, secretion, and has a role in the regulation of lordosis. Additionally, gonadotropin-inhibitory hormone (GnIH) projects to and influences the activity of GnRH neurons in birds. Stress-induced changes in GnIH have been shown to alter breeding behaviors in birds, demonstrating another molecular control of reproduction.
Peripherally, paracrine and autocrine actions within the gonad have been suggested as therapeutic targets for infertility in both males and females. Dysfunction of testicular prostaglandin synthesis is a possible cause of idiopathic male infertility. Indeed, local production of melatonin and corticotropin-releasing hormone (CRH) could influence spermatogenesis via immune pathways in the gonad.
In females, vascular endothelial growth factor A (VEGF-A) has been implicated in an angiogenic process that mediates development of the corpus luteum and thus fertility via the Notch signaling pathway. Age-induced decreases in fertility involve ovarian kisspeptin and its regulation of ovarian sympathetic innervation.
Finally, morphological changes in the arcuate nucleus of the hypothalamus influence female sexual receptivity in rats. The processes mediating these morphological changes have been shown to involve rapid effects of E2 controlling synaptogenesis in this hypothalamic nucleus.
Together, this review highlights new research in these areas, focusing on recent findings in the molecular mechanisms of central and peripheral hormonal control of reproduction. This article is protected by copyright. All rights reserved.
