Identification of α_1b Adrenergic Receptor Protein in Gonadotropin Releasing Hormone Neurones of the Female Rat

Abstract

Noradrenaline is an important neurotransmitter which regulates GnRH release from the median eminence in the female rat during both basal GnRH secretion and the preovulatory or steroid hormone-induced GnRH-mediated LH surge. However, it is not clear at which sites in the brain this predominantly stimulatory influence is exerted nor is it known which adrenergic receptor subtype(s) mediate(s) the effects of noradrenaline. In order to determine if the GnRH neurones in the septum-diagonal band-preoptic area and/or their axon terminals in the median eminence are direct targets for noradrenaline, immunohistochemical triple-labelling studies were conducted to localize simultaneously GnRH peptide, dopamine-beta-hydroxylase and alpha1B adrenergic receptor protein. The results show that about 80% of all GnRH neurones examined contained patches of immunoreactive alpha1B adrenergic receptor protein at or near the plasma membrane and that some of these alpha1B adrenergic receptors were adjacent to dopamine-beta-hydroxylase containing axons. The GnRH neurones which did not contain alpha1B adrenergic receptors were preferentially located in the rostral portion of the septum and diagonal band while all GnRH neurones in the caudal septum, diagonal band and in the preoptic area expressed alpha1B adrenergic receptors. In the median eminence, a few alpha1B adrenergic receptor patches were seen in the external layer and these receptors were only rarely observed to be associated with GnRH containing axon terminals. The results suggest that the effects of noradrenaline on GnRH release are, at least in part, mediated by the activation of alpha1B adrenergic receptors which are located on most GnRH perikarya while the median eminence is not a likely site at which GnRH release is regulated by alpha1B adrenergic receptors.

Loss of Luteinizing Hormone Surges Induced by Chronic Estradiol Is Associated with Decreased Activation of Gonadotropin-Releasing Hormone Neurons1

“…Alternatively, the neural signal to the GnRH neurons is mediated by a number of different neurotransmitters and some of them are not completely suppressed after 4 wk of estradiol treatment. Numerous inputs, both stimulatory and inhibitory, control GnRH release [35][36][37][38], and a plethora of anatomical and pharmacological evidence indicates that there are a number of different subpopulations of GnRH neurons [39][40][41][42][43][44]. Thus, when a given subpopulation of GnRH neurons is blocked, e.g., the neurons activated by estradiol, the action of any residual inputs such as progesterone may be reflected in part by cFos activation of the remaining GnRH neurons.…”

Suppression of Tonic Luteinizing Hormone Secretion and Norepinephrine Release near the GnRH Neurons by Estradiol in Ovariectomized Rats

“…For example, medullary A1 and A2 noradrenergic neurons project to the medial septum-diagonal band/rostral preoptic area [25, 26], the region containing the largest number of GnRH cell bodies [27]. In addition, the GnRH neurons possess adrenergic receptors [28], although the actions of NE may also be mediated by other interneurons [22]. Further, most of the A1 and A2 neurons have estrogen receptors [29, 30], indicating that the anatomical components for an action of estradiol on LH via medullary noradrenergic pathways are in place.…”

Catecholamines in Regulation of Development of GnRH Neurons of Rat Fetuses

“…In adult rats, GnRH-neurons and fibers are innervated by TH-immunoreactive fibers, which are both dopaminergic and noradrenergic (Jennes et al, 1982;Hosny and Jennes, 1998). Some TH-fibers terminated on the bodies of GnRH-neurons are dopaminergic and originate from the periventricular nucleus of hypothalamus, others are noradrenergic and come to the septo-preoptic area from the brain stem (Horvath et al, 1993).…”