Gonadotropin-releasing Hormone Neuronal Function Research Articles

Pulsatile gonadotropin-releasing hormone (GnRH) secretion is an intrinsic function of GnRH neurons, as revealed by the culture of single vomeronasal organ obtained from the embryonic rat

Pulsatile gonadotropin-releasing hormone (GnRH) secretion is an intrinsic function of GnRH neurons, as revealed by the culture of single vomeronasal organ obtained from the embryonic rat

Neuroendocrine control of female puberty: glial and neuronal interactions.

Emerging evidence suggests that, in addition to neuronal inputs, growth factors of glial origin are also important in the control of mammalian puberty via a cell-cell interaction that ultimately affects the neurons that release gonadotropin-releasing hormone (GnRH), a neurohormone controlling sexual development. Among these growth factors, transforming growth factor-alpha (TGF alpha) appears to be one of the physiologic components that controls the onset of female puberty by affecting GnRH neuronal activity in a glia-mediated autocrine/paracrine manner. Specifically, TGF alpha induces glia to produce bioactive substances, such as prostaglandin E2 (PGE2). In turn, PGE2 directly acts on GnRH neurons to stimulate the release of GnRH. Furthermore, the neuroregulin of glial origin neu differentiation factor (NDF) was found to facilitate the action of TGF alpha, suggesting that other growth factors may exert their biologic effects on GnRH neuronal function via a glia/neuron interaction. Another indication that glial cells may be involved in the regulation of neuroendocrine function is the presence of estrogen receptors on hypothalamic astrocytes. Thus, region-specific glial cells appear to play an integral role in the regulation of neuroendocrine function.

Gonadotropin-releasing hormone and gonadotropin in goldfish and masu salmon

Reproductive activities in vertebrates are regulated by an endocrine system, consisting of the brain-pituitary-gonad axis. In teleosts, gonadotropin-releasing hormone (GnRH) in the brain stimulates gonadotropin (GTH) release in the pituitary gland, but because of lack of the portal vessel, it is not known when and how much GnRH is released for the regulation of GTH release. There are multiple molecular types of GnRH in teleosts and several distinct populations of GnRH neurons in the brain. However, we do not know which types and populations of GnRH neurons regulate reproductive activities. Here we summarize our recent studies on GnRH and GTH in masu salmon Oncorhynchus masou and goldfish Carassius auratus. Immunocytochemistry showed the location and molecular types of GnRH neurons. Salmon (sGnRH) and chicken-II GnRH (cGnRH-II) neuronal fibers were widely distributed in the brain of both masu salmon and goldfish. Only sGnRH fibers were observed in the pituitary of masu salmon, whereas both sGnRH and cGnRH-II fibers were observed in the goldfish pituitary, indicating that species specific GnRH profiles are involved in the regulation of pituitary function in teleosts. A series of experiments in masu salmon and goldfish suggest that among GnRH neuron populations GnRH neurons in the ventral telencephalon and the hypothalamus regulate GTH release, and that GnRH of the terminal nerve origin is not essential to gonadal maturation and ovulation. The biological function of other GnRH neurons remains unkown. Two GTHs appear to be characteristic of teleost; however, regulation of reproduction by these GTHs is a question that remains to be elucidated. In salmonid species, it is proposed that GTH I stimulates early gonadal development, whereas GTH II acts in later stages. When GTH expression was examined in goldfish, both GTH I β and II β mRNA levels in the pituitary gland showed increases in accordance with gonadal development, unlike the sequential expression of GTH subunits in salmonids. The expression of these GTH subunit mRNAs were affected by water temperature, starvation, and steroid hormones in goldfish, but in what manner these two GTHs regulate gonadal development remains to be clarified.

Actions of acetyl- L-carnitine on the hypothalamo-pituitary-gonadal system in female rats

Acetyl- L-carnitine (ALC) is known to affect several aspects of neuronal activity. To evaluate the neuroendocrine actions of this compound, several endocrinological parameters were followed in ALC-treated and control animals during recovery from dark-induced anestrus. In treated animals, serum luteinizing hormone (LH) and prolactin levels were higher than those of controls during the proestrous and estrous phases of the cycle, and serum estradiol levels were higher during estrus. No significant changes were observed in serum levels of follicle-stimulating hormone and progesterone. Uterine weight was increased in ALC-treated rats during proestrus and estrus, but not in diestrus. The basal release of gonadotropin-releasing hormone (GnRH) from perifused hypothalamic slices of ALC-treated animals was elevated at proestrus and diestrus, and GnRH release elicited by high K + was higher during all three phases of the cycle. The basal release of LH from perifused pituitaries of treated animals was elevated in diestrus, and the LH response to GnRH was higher in estrus and diestrus I. Depolarization with K + caused increased LH secretion during proestrus and estrus in treated animals. In contrast to these effects of ALC treatment in vivo, no direct effects of ALC were observed during short- or long-term treatment of cultured pituitary cells. These results indicate that ALC treatment influences hypothalamo-pituitary function in a cycle stage-dependent manner, and increases the secretory activity of gonadotrophs and lactotrophs. Since no effects of ALC on basal and agonist-induced secretory responses of gonadotrophs were observed in vitro, it is probable that its effects on gonadotropin release are related to enhancement of GnRH neuronal function in the hypothalamus.