Number Of Luteinizing Hormone Receptors Research Articles

Pituitary and ovarian function in postpartum beef cows. I. Effect of suckling on serum and follicular fluid hormones and follicular gonadotropin receptors.

The effect of suckling on serum and follicular fluid hormones and on follicular gonadotropin receptors was studied. Sixteen anestrous postpartum cows were assigned to 1 of 2 groups: suckled (S) or weaned (W). All calves were allowed to suckle ad libitum from parturition to 21 days postpartum when calves from W cows were weaned. All cows were ovariectomized on Day 25 postpartum. W cows had more (P less than 0.01) pulses of LH during the 96-h period from weaning until ovariectomy than S cows (6.3 vs. 1.3 pulses). Serum concentrations of prolactin (Prl), estrone (E1), estradiol-17 beta (E2) and progesterone (P) were not different (P greater than 0.10) between groups. Furthermore, there were n differences (P greater than 0.10) in follicular in contents of luteinizing hormone (LH), E1, E2 and P between the treatment groups. However, follicular fluid content of Prl was greater (P less than 0.05) in the W cows than in the S cows (123 vs. 65.1 ng/cow). The number of follicular LH receptors was greater (P less than 0.05) in the W cows than in the S cows (71.1 vs. 48.3 fmoles/mg protein) although the number of follicular follicle-stimulating hormone (FSH) receptors was not different (P greater than 0.10) between W cows and S cows (1531 vs. 1862 fmoles/mg protein). There were no correlation between serum hormone concentrations and follicular fluid hormone content; however, the numbers of follicular LH receptors and follicular fluid Prl content were highly correlated in the W cows (r = 0.85; P less than 0.05). It is concluded that removal of the suckling stimulus increases pulsatile LH release and the accumulation of Prl in the follicular fluid. These factors, either together or separately, may at least in part be responsible for the increase in follicular LH receptor concentrations that were observed in the W cows.

HCG stimulation of testicular LHRH-like activity.

It is well established that the administration of high doses of luteinizing hormone (LH) or human chorionic gonadotropin (HCG) to animals can impair gonadal function in both the male and female. These effects can be duplicated by the administration of LH releasing hormone (LHRH) or its agonists to intact animals, including man. Somewhat surprisingly, recent results have demonstrated that similar impairment of gonadal function by LHRH and its agonists can be achieved in the absence of the pituitary (for review see ref. 7), and the demonstration of specific, high-affinity binding sites for LHRH and its agonists on ovarian luteal cells and on testicular Leydig cells, could mean that LHRH-like factors are involved in the local regulation of the gonads. A further intriguing finding is the striking similarity between the direct, inhibitory effects of LHRH and LH/HCG on the gonads; for example, both treatments reduce LH receptor numbers and the steroidogenic responsiveness of rat Leydig cells. We now offer a possible explanation for this similarity by demonstrating that HCG treatment stimulates the testicular production of a biologically active LHRH-like factor, suggesting that the inhibitory actions of HCG on the Leydig cell may be mediated by the local production of this factor.

Prolactin, testicular growth and LH receptors in the ram following light and 2-Br-alpha-ergocryptine (CB-154) treatments.

The influence of prolactin (PRL) on testicular growth and luteinizing hormone receptors (LH-R) in the ram has been investigated. Unoccupied LH-R were estimated in the 5000 X g testicularmembrane fraction.The specificactivityof the (‘25Il-oLH (enzymatically radioiodinated) was 20-40 �iCi4tgand maximum binding activityreached 15-25%. Kinetic curves indicated that incubation for 20 h at 20#{176}C was the optimum condition to obtain the maximum specific binding activity. Enzymatic treatmenthas demonstrated the lipoprotein structure of the LH-R. The specificityof the assay was confined to LH or human chorionic gonadotropin molecules. The equilibrium associationconstant (Ka) of the LH/receptor interactionwas 10i0 M -i and the number of LH-R determined using Scatchard analysis was “vS fmoles/mg membrane protein.The precision of the assay was 18%. Plasma prolactin levelsdecreased by CB-154 treatment or increasedby photostimulation did not change either the LH-R number or the equilibrium association constant. However, in the two experiments, a delay in the beginning of testiculargrowth was observed in rams treatedwith CB154. In contrast to what has been found in rodents,these resultssuggest that,in the case of seasonal variations,high plasma prolactin levelsinfluencechanges in testicularactivity without any involvement of the speculated regulationby prolactinof the LH-R number.

Estrogen dependence of a gonadotropin-induced steroidogenic lesion in rat testicular Leydig cells.

Leydig cells isolated from the testes of rats treated with intravenous exogenous gonadotropin (hCG) or subcutaneous gonadotropin-releasing hormone (GnRH) show markedly decreased luteinizing hormone (LH) receptors and a partial block in testicular 17,20 desmolase activity. In contrast, Leydig cells from animals with equivalent degrees of LH receptor loss induced by subcutaneous hCG treatment show no change in 17,20 desmolase activity. These findings indicated that the acuteness of gonadotrophic stimulation, rather than the extent of LH receptor loss, was responsible for the steroidogenic lesion. A role of estradiol in the enzymatic block produced in vivo by acute elevation of circulating gonadotropin (intravenous hCG or GnRH-stimulated endogenous LH) was suggested by rapid elevations of testicular 17beta-estradiol within 30 min after intravenous hCG, whereas more gradual increases in estradiol occurred 4-8 h after subcutaneous hCG. The inhibitory effect of endogenous estrogen on testicular steroidogenesis was confirmed by the ability of an estrogen antagonist (Tamoxifen) to prevent the reduction of testosterone responses caused by intravenous hCG and subcutaneous GnRH. In addition, Tamoxifen significantly increased the number of LH receptors in Leydig cells from both control and gonadotropin-desensitized animals. These findings indicate that the acute elevations of intratesticular estrogen produced by treatment with hCG or GnRH are responsible for the steroidogenic lesion seen in gonadotropin-desensitized Leydig cells. These results also suggest that locally produced estrogens contribute to the regulation of testicular LH receptors and 17,20 desmolase activity.

Gonadotropin-induced regulation of luteinizing hormone receptors and desensitization of testicular 3':5'-cyclic AMP and testosterone responses.

Administration of human chorionic gonadotropin (hCG) to male rats was followed by dose-related changes in luteinizing hormone (LH) receptors in the testis. After treatment with a low dose of hCG (10international units), the number of LH receptors increased slightly over the first 24 hr, then fell to about 30% of the control value. These changes occurred with occupancy of only 8% of the available receptors, and were initially accompanied by increased basal testosterone production in vitro with no change in basal 3'5'-cyclic AMP production. During stimulation with hCG in vitro, such testes showed a transient decrease in cyclic AMP response on the first day after gonadotropin treatment and no change in testosterone response. By contrast, a 20-fold higher dose of hCG caused more rapid and complete loss of LH receptors, with major and transient occupancy of receptors at 24 hr and marked elevations of basal cyclic AMP and testosterone production in vitro. The initial occupancy of receptors was accompanied by a rapid fall in the cyclic AMP response to hCG in vitro, and was followed by marked receptor loss and inhibition of the cyclic AMP response for up to 5 days. The testosterone response to hCG in vitro was completely inhibited for about 3 days, then rose to the control level at 5 days, when only a small proportion of the original receptor sites and cyclic AMP response had begun to return. Such complete recovery of the steroidogenic response when only a fraction of the receptor population had returned was consistent with the presence of receptor reserve or "spare" receptors in the testis. These studies have demonstrated that negative regulation of LH receptors by exogenous gonadotropin is accompanied by consequent changes in cyclic AMP and testosterone responses to hCG in vitro. Hormone induced desensitization of interstitial cell responses was initially related to occupancy of LH receptors and later to a protracted loss of receptor sites.