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FSHR与LHR的研究进展   总被引:3,自引:0,他引:3  
本文重点论述了FSHR与LHR的结构及在卵母细胞体外成熟过程中的表达和调控,并阐述了FSHR与LHR的研究现状及存在的问题。  相似文献   

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In vitro responsiveness of the horse anterior pituitary (AP) gonadotropes to single and multiple GnRH challenges was examined. The pituitaries were collected from reproductively sound mares in estrus (n = 5) and diestrus (n = 5). Uniform 0.5 mm AP slices were subdivided using a 3 mm biopsy punch and then bisected for use in the perifusion chamber. Four bisected sections per chamber were perifused at 0.5 ml/min at 37 C for 560 min in Medium 199 saturated with 95% 0(2)/5% CO2. Ten minute fractions were collected after an initial 2 hr equilibration period. Four different treatment regimes of GnRH (10(-10) M) were evaluated: (A) three consecutive 10 min GnRH pulses separated by 80 and 100 min, respectively; (B) a single 120 min GnRH infusion; (C) a 10 min GnRH pulse followed 80 min later by a 120 min GnRH infusion and (D) two 10 min GnRH pulses separated by 60 min followed 80 min later by a 120 min GnRH infusion. Estimated total pituitary LH content was higher in estrous than diestrus mares (p less than 0.05). The total amount of LH released in response to GnRH tended to be greater in estrus than diestrus (p less than 0.1), whereas the percentage of LH released in estrus and diestrus was similar. An increase in the area under the LH response curve was noted with each successive 10 min pulse of GnRH during both estrus and diestrus (p less than 0.05), demonstrating a self-priming effect of GnRH. In addition, a significant increase in the peak LH amplitude (p less than 0.05) and the slope to peak amplitude (p less than 0.05) were observed for the 120 min GnRH pulse in regime C and D indicating that prior exposure to short-term pulses of GnRH increased the acute LH secretory response. These results suggest that in the cycling mare (1) the responsiveness of the pituitary (amount of LH released as percent of total LH) is similar in both estrus and diestrus, however, the magnitude of the LH response (total microgram amount of LH released) differs with the stage of the estrous cycle, being highest in estrus, and appears to be related, in part, to pituitary LH content and (2) GnRH self-priming occurs independently of the stage of the estrous cycle. Furthermore, we have demonstrated that the pulsatile mode of GnRH can act directly on the anterior pituitary to dictate the pulsatile release pattern of LH in the cycling mare.  相似文献   

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The secretion of luteinizing hormone-releasing hormone (LHRH) and its temporal association with pulses of luteinizing hormone (LH) was examined in ovariectomized prepuberal gilts. Push-pull cannulae (PPC) were implanted within the anterior pituitary gland and LHRH was quantified from 10 min (200 microliters) perfusate samples. Serum LH concentrations were determined from jugular vein blood obtained at the midpoint of perfusate collection. Initial studies without collection of blood samples, indicated that LHRH secretion in the ovariectomized gilt was pulsatile with pulses comprised of one to three samples. However, most pulses were probably of rapid onset and short duration, since they comprised only one sample. Greater LHRH pulse amplitudes were associated with PPC locations within medial regions of the anterior pituitary close to the median eminence. In studies which involved blood collection, LH secretion was not affected by push-pull perfusion of the anterior pituitary gland in most gilts, however, adaptation of pigs to the sampling procedures was essential for prolonged sampling. There was a close temporal relationship between perfusate LHRH pulses and serum LH pulses with LHRH pulses occurring coincident or one sample preceding serum LH pulses. There were occasional LHRH pulses without LH pulses and LH pulses without detectable LHRH pulses. These results provide direct evidence that pulsatile LHRH secretion is associated with pulsatile LH secretion in ovariectomized gilts. In addition, PPC perfusion of the anterior pituitary is a viable procedure for assessing hypothalamic hypophyseal neurohormone relationships.  相似文献   

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Seventy crossbred heifers were allotted randomly to 10 treatment groups. Treatments consisted of active immunization against ovalbumin (OV) conjugates of luteinizing hormone-releasing hormone (LHRH), human chorionic gonadotropin (hCG) and bovine luteinizing hormone (bLH) with each of three adjuvants. The adjuvants were complete Freund's adjuvant (CFA), M103(6) and 6VR6. Control animals were immunized against OV alone using CFA. Bulls were placed with the heifers following immunization to allow comparison of pregnancy rates between groups. Blood samples were collected weekly for 14 wk to determine antibody concentrations. Significant levels of circulating LH or LHRH antibodies were detected in heifers immunized with each of the hormone conjugates. Complete Freund's adjuvant was the most effective for stimulating antibody response to these antigens; however, M103 was equally effective when used with bLH or hCG conjugates. None of the heifers in the bLH-OV-CFA, bLH-OV-M103 or LHRH-OV-CFA immunization groups was pregnant at slaughter, whereas 71% of the OV-CFA control heifers were pregnant. Fertility suppression may be achieved in the bovine by active immunization against any of these three hormone conjugates. However, the duration of this study (8 wk after immunization) does not allow evaluation of the duration of effectiveness of each of the treatments.  相似文献   

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The objective was to determine how estradiol (0 vs 1 mg) and changes in the dosage of luteinizing hormone releasing hormone (LHRH; 1,000 ng/steer vs 1 ng/kg body weight) and frequency of LHRH injection (25 vs 50 min) affect LH and follicle stimulating hormone (FSH) release in steers. In steers pretreated with estradiol peak concentrations of LH in serum after LHRH averaged 14.4 ng/ml, which was greater (P less than .001) than peak concentrations in steers given oil (7.4 ng/ml). Increasing the dosage of LHRH from 1 ng/Kg body weight (approximately or equal to 300 ng/steer) to 1,000 ng/steer increased (P less than .001) peak LH values from 7.5 to 14.4 ng/ml. Furthermore, increasing the frequency of LHRH injections from once every 50 min to once every 25 min increased (P less than .001) LH release, but only in steers given estradiol. Estradiol reduced basal concentrations of FSH by 65% and then increased LHRH-induced FSH release by 276% (P approximately .07) relative to values for steers given oil. Only when 1,000 ng LHRH was given every 25 min to steers pretreated with estradiol were LH and FSH release profiles similar to the preovulatory gonadotropin surges of cows in magnitude, duration and general shape. The results demonstrate that increases in the dosage or frequency of LHRH pulses increase LHRH-induced release of LH, but not of FSH. Furthermore, these results are consistent with the hypothesis that in cows, estradiol increases responsiveness of the gonadotrophs to LHRH and then increases the magnitude and frequency of pulses of LHRH secretion beyond basal levels, thereby causing the preovulatory gonadotropin surges.  相似文献   

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We tested the hypothesis that rapidly expressed inhibitory effects of estradiol (E) on luteinizing hormone (LH) release in the male are attributable, in part, to suppression of luteinizing hormone-releasing hormone (LHRH) release. Hypophyseal-portal cannulated, castrated male sheep were infused with E (15 ng/kg/hr) or vehicle. Portal and jugular blood samples were collected at 10-min intervals for 4 hr before, and for either 12 hr (E, n = 4; vehicle, n = 4) or 24 hr (E, n = 8; vehicle, n = 3) after the start of infusion. In animals sampled for 16 hr, temporal changes in both LHRH and LH were assessed. In animals sampled for 28 hr, only LH data were analyzed. Before either the 12-hr or 24-hr infusion, LHRH and/or LH mean concentrations, pulse amplitude and interpulse interval (IPI) did not differ between E- and vehicle-infused animals. In animals sampled for 16 hr, no effects of time or steroid × time interactions were detected for mean LHRH and LHRH pulse amplitude; however, both were greater (P < 0.01) in vehicle-infused than in E-infused males. LHRH IPI was unaffected by infusion. In contrast, both mean LH and LH pulse amplitude declined (P < 0.01) within 4–8 hr after the start of E infusion, whereas mean LH IPI was unaffected. In animals sampled for 28 hr, an effect of time (P < 0.01) and a steroid × time interaction (P < 0.01) was detected for mean LH, and there was an effect of time (P < 0.01) on LH pulse amplitude. Mean LH IPI was not affected. Our results show that in male sheep E rapidly reduces LH release in the absence of a detectable change in LHRH release.  相似文献   

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Cyclic changes in serum concentration of luteinizing hormone (LH) were observed throughout the estrous cycle of Asiatic elephants (Elephas maximus). The increase in serum LH was correlated with a slight increase in serum estradiol concentration and the onset of behavioral heat (willingness to mate). In a second series of studies, injection of luteinizing hormone-releasing hormone after 3 days of estrone administration induced an increase in serum LH. These studies indicate that the Asiatic elephant exhibits a cyclic LH release that can be experimentally induced by estrone and luteinizing hormone-releasing hormone administration.  相似文献   

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The requirement for endogenous LHRH and LH action in the maintenance of elevated plasma concentrations of testosterone in bulls receiving the LHRH agonist deslorelin was examined. In Experiment 1, bulls were either (i) left untreated (control); (ii) implanted with deslorelin; (iii) actively immunized against LHRH; or (iv) implanted with deslorelin and immunized against LHRH. Experiment 2 was of similar design to Experiment 1, except that bulls were immunized against LH in place of LHRH. In Experiment 1, plasma LH declined in bulls immunized against LHRH, but not in the bulls immunized against LHRH and implanted with deslorelin. Also in Experiment 1, plasma testosterone declined in bulls immunized against LHRH but was elevated in bulls treated with deslorelin and bulls treated with deslorelin and immunized against LHRH. In Experiment 2, bulls immunized against LH and treated with deslorelin had plasma concentrations of testosterone similar to controls, whereas bulls treated only with deslorelin had elevated plasma testosterone. It was concluded from these experiments that endogenous LHRH action was not required for increased steroidogenic activity in bulls treated with a LHRH agonist. However, circulating LH was necessary for increased plasma testosterone in bulls implanted with deslorelin. LH is therefore involved in mediating the response of bulls to treatment with deslorelin, either by acting directly at the testes or through a permissive role that allows a direct action of deslorelin at the testes.  相似文献   

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Administration of endotoxin suppresses circulating concentration of luteinizing hormone (LH) in a number of species, including rats, sheep, cattle, and non-human primates. Specifically, endotoxin administration decreases circulating concentration of LH and LH pulses frequency in castrated male sheep. Endotoxin could alter circulating concentrations of LH via actions at the hypothalamus through altered GnRH production and/or release, or endotoxin could alter circulating concentrations of LH at the level of the pituitary via inhibition of LH production and release or inhibition of LH in response to GnRH. The site of endotoxin suppression of circulating concentrations of LH as well as possible mediators of endotoxin suppression of circulating concentrations of LH, including cortiocotropin-releasing hormone, arginine vasopressin, glucocorticoids, inflammatory cytokines, prostaglandins, and opioids, are discussed.  相似文献   

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GPR30 is known as a membrane receptor for picomolar concentrations of estradiol. The GPR30-specific agonist G1 causes a rapid, non-genomic suppression of gonadotropin-releasing hormone (GnRH)-induced luteinizing hormone (LH) secretion from bovine anterior pituitary (AP) cells. A few studies have recently clarified that protein kinase A (PKA) and phosphorylated extracellular signal-regulated kinase (pERK) might be involved in cytoplasmic signaling pathways of GPR30 in other cells. Therefore, we tested the hypothesis that PKA and ERK kinase (MEK) are important cytoplasmic mediators for GPR30-associated non-genomic suppression of GnRH-induced LH secretion from bovine AP cells. Bovine AP cells (n = 8) were cultured for 3 days under steroid-free conditions. The AP cells were previously treated for 30 min with one of the following: 5000 nM of PKA inhibitor (H89), 1000 nM of MEK inhibitor (U0126), or a combination of H89 and U0126. Next, the AP cells were treated with 0.01 nM estradiol for 5 min before GnRH stimulation. Estradiol treatment without inhibitor pretreatment significantly suppressed GnRH-induced LH secretion (P < 0.01). In contrast, estradiol treatment after pretreatment with H89, U0126 or their combination had no suppressive effect on GnRH-induced LH secretion. The inhibitors also inhibited the G1 suppression of GnRH-induced LH secretion. Therefore, these data supported the hypothesis that PKA and MEK (thus, also pERK) are the intracellular mediators downstream of GPR30 that induce the non-genomic suppression of GnRH-induced LH secretion from bovine AP cells by estradiol or G1.  相似文献   

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This study was conducted to determine the correlation between reproductive hormones and musth in a male African elephant. Changes in circulating luteinizing hormone (LH), follicle stimulating hormone (FSH), testosterone and immunoreactive (ir-) inhibin and the degree of musth were evaluated for 4 years. LH increased 4 weeks before musth began. The highest concentrations of testosterone and ir-inhibin were observed from April to October. There were positive correlations among testosterone, ir-inhibin and musth behavior. These findings suggested that the surge-like LH in the pre-musth period might stimulate secretion of testosterone and ir-inhibin and thus initiate the musth behavior. This study also suggested that the high LH level before musth might be a useful biomarker for the beginning of the musth season.  相似文献   

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This investigation characterized serum concentrations of luteinizing hormone (LH), estradiol-17 beta (E2), progesterone (P4) and cortisol (C) in anestrous sows. Twenty-two sows that had not returned to estrus within 45 days after weaning (anestrous sows), and ten sows that had returned to estrus within seven days following weaning (cyclic sows) were nonsurgically fitted with indwelling jugular vein cannulae. Blood samples were collected at 6 h intervals for seven days and at 15 min intervals for 8 h on the fifth day after cannulation. Serum LH concentrations were determined in all samples, while C, E2 and P4 levels were quantitated in serum collected at 6 h intervals. Serum P4 concentrations in anestrous sows were consistently less than 0.5 ng/mL, and E2 levels ranged from 10 to 19 pg/mL. Concentrations of LH remained less than 1.0 ng/mL in anestrous sows, whereas a preovulatory LH surge was observed in five of ten cyclic sows. There was a circadian rhythm in mean C levels with C peaks occurring at 0600 or 2400 h and nadir levels observed at 1200 and 1800 h. Few differences in C levels were detected between anestrous and cyclic sows. It was evident that anestrous sows did not exhibit cyclic or predictable variations in steroid hormone concentrations. Unfortunately, the results of this study failed to elucidate the endocrine pathogenesis of the anestrous sow.  相似文献   

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The effect of the luteinizing hormone (LH) on the oogenesis of ovaries from newly-hatched chicks treated in vivo on days 13, 15, and 17 of embryonic development was analyzed. Changes in oogonial proliferation, meiotic prophase, degeneration of germ cells, and primordial follicular organization were determined. Results indicate that the total number of germ cells was not affected by the LH treatment, but significant differences existed in the number of oogonia and oocytes between the ovaries of control and LH-treated chicks. LH treatment increased the percentage of oocytes and diminished the percentage of oogonia. The mitotic activity of oogonia and degeneration of germ cells decreased, but the number of follicles during development increased in LH-treated ovaries. These findings suggest that LH treatment might trigger a cascade of endocrine events, resulting in inhibition of oogonial proliferation and induction of the meiotic prophase and follicle formation.  相似文献   

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The objective of the present study was to determine if postpubertal boars (12-13 months of age; 156 +/- 8 kg) with large testes had altered hypothalamic control of secretion of luteinizing hormone (LH). Seven boars with the highest estimated 150 d, paired testis weights from a line selected for large testes (769 +/- 60 g = mean weight of excised testes) and 8 boars from a control group (control, 544 +/- 20 g) were tethered in stalls and fitted with indwelling jugular catheters. Males were bled when they were intact, 14 days after castration and during administration of sodium pentobarbital anesthetic (subsequent to castration) to block secretion of endogenous LH-releasing hormone (LHRH). Blood samples were collected at 12-min intervals for 6 hr before and 1 hr after intravenous injection of LHRH in intact and castrated males. During anesthesia, LHRH was administered 4 times at 1-hr intervals and blood samples were collected every 6 min. All samples were analyzed for concentrations of LH and pooled samples were analyzed for concentrations of 17-beta estradiol (E2) and testosterone (T). In intact and castrated males, mean concentrations of LH, frequency and amplitude of pulses of LH, and concentrations of E2 and T were not different between boars of the two groups (P greater than .10). Response to exogenous LHRH was less (P less than .05) in intact males with large testes than in corresponding males from the control group (P less than .05). Fourteen days after castration, males that had larger testes before castration had less of a response to LHRH than males from the control group (P less than .05).(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

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