Properties and Regulation of GnRH Receptors in the Anterior Pituitary and the Testis of the Rat: Different Response of Leydig Cell LH and GnRH Receptors to Hormonal Treatments

Abstract

The properties (association and dissociation rates, affinity and specificity) of GnRH receptors in the rat pituitary and the Leydig cells are very similar. In addition, in vivo administration for 5 or 11 days of 10 micrograms of GnRH to adult rats resulted in an increase (p less than 0.01) in both Leydig cell and pituitary GnRH receptors. In contrast, the same treatment caused a significant decrease (p less than 0.01) of Leydig cell LH receptor number. Furthermore, testosterone propionate (500 micrograms/day), which had no effect on Leydig cell LH receptors, caused a significant increase (p less than 0.01) of testicular GnRH receptors but a decrease (p less than 0.01) of pituitary GnRH receptors. Estradiol 17 beta valerate (5 micrograms/day) reduced (p less than 0.01) both testicular (5 days) and pituitary (5 and 11 days) GnRH receptors. Such treatment for 5 days also decreased (p less than 0.05) the Leydig cell LH receptors. No effect of dexamethasone and 17-hydroxyprogesterone was seen after 5 or 11 days of treatment. Thus, although pituitary and Leydig cell receptors appear similar, their regulation by exogenous hormone treatments is different. Furthermore, the regulation of Leydig cell GnRH and LH receptors also appears very different, suggesting different roles of the receptors in the control of the Leydig cell function.

Androgen Regulates Follicle-Stimulating Hormone β Gene Expression in an Activin-Dependent Manner in Immortalized Gonadotropes

“…Studies using rats have most commonly demonstrated that the levels of GnRH-R and GnRH-R gene expression are reduced by androgen treatment (18)(19)(20). However, this does not appear to be the case in the mouse.…”

“…In addition to modulating the activin/FS system in the pituitary, androgens have been shown to regulate GnRH sensitivity via alterations in the level of GnRH-Rs (16)(17)(18)(19)(20). In fact, in the case of the LH␤ gene, GnRH stimulation was required to observe androgen repression in the L␤T2 cell model (9,10).…”

“…In addition to these actions of androgen on FSH␤ transcription, androgens have been shown to modulate levels of follistatin (FS) in the rat pituitary in vivo and both activin and FS in cultured rat pituitary cells (8,14,15), indicating that the mechanism of androgen action on FSH␤ might be indirect, through modulation of the activin/FS system in the pituitary. Furthermore, GnRH receptor (GnRH-R) within the pituitary of rodents is modulated by androgens (16)(17)(18)(19)(20), which in turn may alter responsiveness of FSH␤ to GnRH, and thus act as another indirect mechanism through which androgens regulate FSH␤ expression at the level of the pituitary. Because androgens stimulate GnRH-R expression in mouse pituitary (9,21), in contrast to the inhibitory effect most commonly observed in rats (18)(19)(20), androgens may stimulate mouse FSH␤ gene expression through multiple mechanisms, including via enhancing responsiveness of FSH␤ to GnRH.…”

Alzheimer?s disease: the impact of age-related changes in reproductive hormones

“…Indeed, these receptors have been shown to elicit signals central to the growth and development, maintenance and normal functioning, as well as the degeneration of the brain. At the present time, it is difficult to determine whether the effects ascribed to a particular HPG hormone with regard to neuronal structure and function are mediated via its own receptor signaling, or via feedback regulation on other HPG hormone receptors; such is the case for estrogen modulation of GnRH, gonadotropin and progesterone receptor expression in neuronal cells [124,139,153]. Likewise, it is not clear to what extent the above cognitive and functional observations are due to one hormone per se (e.g.…”

RFamide‐related peptide 3 and gonadotropin‐releasing hormone‐II are autocrine–paracrine regulators of testicular function in the boar

“…Negative feedback of gonadal steroids and inhibin at the hypothalamus and anterior pituitary gland was thought to be the primary regulator of gonadotropin secretion in pigs (Ford, Klindt, & Wise, ). Neuropeptides and their receptors are also expressed in the gonad, and can directly affect gonadal function (Iwashita & Catt, ; Jegou, Brekke, Naess, Torjesen, & Hansson, ; Kakar, Musgrove, Devor, Sellers, & Neill, ; Nikula & Huhtaniemi, ; Petersson, Emons, & Hammar, ); however, information indicating that neuropeptides may act as paracrine regulators of testicular function in the boar is lacking. Here, we review and present evidence that RFamide peptides, the products of the NPVF gene, are not major hypophysiotropic hormones in the pig, but could be important paracrine factors in the negative regulation of testosterone secretion in boars.…”