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1.
Involvement of endogenous opioids in inhibition of luteinizing hormone (LH) release and stimulation of prolactin (PRL) release was investigated by injecting the opioid antagonist naloxone into 18 ewes on d 7 and 8, d 12 and 13, and d 18 and 19 postpartum. Compared with control injections of saline, iv naloxone (1 mg/kg) increased serum concentrations of LH and decreased serum PRL in samples collected 15, 30 and 45 min after each injection. Ewes lambing in the spring (March) or autumn (September and October) that nursed one or two lambs did not differ in their LH and PRL responses to naloxone. Autumn-lambing ewes from which lambs were weaned within 1 d after parturition did not differ from ewes of the autumn-nursed group in any of the following characteristics: 1) serum LH increases following naloxone, 2) basal secretion of LH, 3) postpartum interval to first increase in serum progesterone and 4) relative decrease in serum PRL after naloxone despite large differences in basal PRL secretion. In summary, postpartum expression of a naloxone-reversible inhibition of LH release and stimulation of PRL secretion did not depend on suckling stimuli or differ between autumn and spring parturitions.  相似文献   

2.
Two experiments were conducted in ovariectomized, pituitary stalk-transected ewes to determine if dopamine (DA), norepinephrine (NE) or serotonin (5-HT) alter secretion of luteinizing hormone (LH), follicle-stimulating hormone (FSH) and prolactin (PRL). In experiment 1, ewes were infused (iv) with saline (control), DA (66 micrograms/kg/min), NE (6.6 micrograms/kg/min) or 5-HT (6.6 micrograms/kg/min). Treatments did not alter pulse frequency, but 5-HT increased (P less than .05) amplitude of pulses of LH and mean concentrations of LH, DA and NE were without effect on basal secretion of LH. DA but not NE or 5-HT decreased (P less than .05) the release of LH in response to gonadotropin hormone-releasing hormone (GnRH, 25 micrograms, im). Concentrations of FSH were not affected by treatments. Secretion of PRL was reduced (P less than .05) by treatment with DA and NE but not 5-HT. Each amine reduced (P less than .05) the release of PRL in response to thyrotropin-releasing hormone (TRH; 3 micrograms, im). In experiment 2, ewes were given DA at doses of 0, 0.66, 6.6 or 66.0 micrograms/kg/min, iv. No dose altered basal LH, but each dose reduced (P less than .05) basal and TRH-induced release of PRL. Key findings from these studies include direct pituitary action for: (1) 5-HT enhanced basal secretion of LH, (2) suppression of GnRH-induced secretion of LH by DA. (3) DA and NE inhibition of PRL secretion, and (4) DA, NE and 5-HT inhibition of release of PRL in response to TRH.  相似文献   

3.
To examine the effect of diet on luteinizing hormone (LH) secretion, basal and luteinizing hormone releasing hormone (LHRH)-induced LH release was compared in intact or castrated-estradiol-17 beta implanted Finn-Dorset lambs. Ten to 12 wk old ram (n = 20) and ewe lambs (n = 20) were maintained under a 8L:16D photoperiod and fed for high (HG, 163 to 168 g/d) or low (LG, 76 to 103 g/d) rates of gain. Eight to 10 wk later, baseline LH concentrations were determined in blood samples collected at 20 min intervals for 7 h. The following day, lambs were given an iv injection of 5 micrograms of estradiol-17 beta followed within 4 h by LHRH (.5 or 2.5 micrograms). Baseline concentrations of LH for HG ewes were threefold greater than for LG ewes (4.2 vs 1.4 ng/ml), respectively. Time to peak response was inversely related to dietary energy level (P less than .025). Basal LH levels were similar across diets in rams. Total LH release following LHRH was dose-dependent (P less than .005). Effects of gonadal feedback were tested in a second group (n = 24) of castrated lambs. Changes in LH secretion were not different between diets within 3 to 4 wk after castration. A subcutaneous silastic implant (22 mm) of estradiol-17 beta inhibited (P less than .01) LH concentrations across diets in both ewes and rams. No differences in estradiol feedback on LH secretion (at the dose of steroid tested) were detected between HG and LG lambs. Within 8 d, however, basal LH concentrations were 60% lower (P less than .01) in HG vs LG ewes. Furthermore, peak LHRH-induced LH release was greater (P less than .025) in LG vs HG lambs of both sexes. Estradiol inhibited basal LH secretion in ewes and rams but facilitated LH release in lambs with a reduced rate of gain.  相似文献   

4.
The present studies were undertaken to examine the influence of mu (beta-endorphin, DAMGO, FK 33-824), delta (met-enkephalin, leu-enkephalin, DPLPE) and kappa opioid receptor agonists (dynorphin A, dynorphin B, U 50488) used at different doses (1-1000 nM) alone and in combination with LH (100 ng/ml) on steroidogenesis in porcine granulosa cells derived from large follicles. The effects of mu, delta and kappa receptor agonists on both basal and LH-induced progesterone (P4) secretion were negligible. Agonists of mu opioid receptors reduced basal androstenedione (A4), testosterone (T) and oestradiol (E2) release. Co-treatment with LH entirely abolished the inhibitory effect of these agonists on A4 and E2 secretion and resulted in an increase in T release. The addition of delta receptor agonists was followed by a decrease in basal A4, T and E2 secretion. The cells incubated in the presence of LH increased the androgen production and abrogated the inhibitory effect of delta agonists on E2 output. Basal A4, T and E2 release was also suppressed by kappa receptor agonists. The presence of LH in culture media extended the inhibitory effect of these opioids on E2 output and caused either abolition of the inhibitory influence of kappa agonists or even augmentation of both androgen release in response to the opioids. In conclusion, these data support the involvement of three major types of opioid receptors in the regulation of porcine granulosa cell steroidogenesis.  相似文献   

5.
Three experiments were conducted to examine the relationship between systemic concentrations of luteinizing hormone (LH) and estradiol-17 beta (E2) after withdrawal of progesterone in cycling ewes. In Exp. 1, ewes were assigned randomly to one of three treatments: laparotomy (C), removal of the luteal ovary (ULO), or ULO plus anesthesia with sodium pentobarbital for 6 h beginning 4 h after surgery. Anesthesia was used in an attempt to block the expected increase in tonic secretion of LH. Patterns of LH and E2 in these three groups did not differ during the 24-h experimental period. In Exp. 2, a longer period of anesthesia was utilized. Forty-eight ewes were assigned at random to one of four treatments: C, ULO, lutectomy or an intrafollicular injection of prostaglandin F2 alpha (PGF2 alpha). One-half of the ewes in each group were anesthetized with sodium pentobarbital from initiation of treatment (0 h) until 10 h after surgery. Sodium pentobarbital did not suppress the increases in LH and E2 after progesterone withdrawal. The regression of concentrations of E2 on concentration of LH was not significant. In Exp. 3, ewes were infused with either saline or dopamine after receiving an im injection of PGF2 alpha. Tonic secretion of LH increased after 4 h in ewes infused with saline, but not in ewes infused with dopamine. Despite the suppression of LH, concentrations of E2 increased in dopamine-treated ewes as in control ewes. Therefore, the initial increase in E2 after a decline of progesterone in cycling ewes is independent of increases in LH.  相似文献   

6.
Concentrations of histamine were quantified by an enzymatic isotopic assay in different regions of the brain and pituitary gland of gonadal-intact and chronically ovariectomized ewes during the anestrous season. Sera concentrations of LH were confirmed to be elevated in ovariectomized compared with intact animals immediately before tissues were obtained. Areas of the brain that were examined included cerebral cortex, thalamus, pineal gland, hypothalamus (rostral, medial basal, median eminence), midbrain, cerebellum and brain stem. Concentrations of histamine were greatest within the thalamus, pineal gland, medial basal hypothalamus and median eminence. Histamine within the medial basal hypothalamus was greater (P less than .05) in ovariectomized than in ovarian-intact animals. Further experiments were designed to determine the effect of antihistaminic drugs on secretion of LH. Ovariectomized ewes were treated every 6 h (i.m.) for 24 h with diphenhydramine (an antagonist of the H1-receptor for histamine), cimetidine (an H2-receptor antagonist), a combination of the drugs, or vehicle. Twelve hours after initiation of treatments, animals were injected with estradiol. Diphenhydramine depressed (P less than .01) basal serum concentrations of LH and the positive feedback effect of estradiol on serum concentrations of LH. Cimetidine did not influence the pattern of secretion of LH. Diphenhydramine did not alter LHRH-induced release of LH in ovariectomized ewes or basal serum concentrations of LH in ovarian-intact anestrous ewes. We suggest that histamine acts at the level of the central nervous system through an H1-receptor mechanism to control secretion of LH in female sheep.  相似文献   

7.
Background: Immune stress induced by lipopolysaccharide(LPS) influences the gonadotropin-releasing hormone(GnRH)/luteinizing hormone(LH) secretion. Presence of LPS interacting Toll-like receptor(TLR) 4 in the hypothalamus may enable the direct action of LPS on the GnRH/LH secretion. So, the aim of the study was to investigate the influence of intracerebroventricular(icv) injection of TLR4 antagonist on GnRH/LH secretion in anestrous ewes during LPS-induced central inflammation. Animals were divided into three groups icv-treated with: Ringer-Locke solution, LPS and TLR4 antagonist followed by LPS.Results: It was demonstrated that TLR4 antagonist reduced LPS-dependent suppression of GnRH gene expression in the preoptic area and in the medial basal hypothalamus, and suppression of receptor for GnRH gene expression in the anterior pituitary gland. It was also shown that TLR4 antagonist reduced suppression of LH release caused by icv injection of LPS. Central administration of LPS stimulated TLR4 gene expression in the medial basal hypothalamus.Conclusions: It was indicated that blockade of TLR4 prevents the inhibitory effect of centrally acting LPS on the GnRH/LH secretion. This suggests that some negative effects of bacterial infection on the hypothalamic-pituitary-gonadal axis activity at the hypothalamic level may be caused by central action of LPS acting through TLR4.  相似文献   

8.
Effects of domperidone, a peripheral dopamine receptor antagonist, on secretion of LH and prolactin were studied during the luteal phase and following administration of PGF2 alpha. Since hyperprolactinemia has been reported to inhibit secretion of LH in ewes, effects of thyrotropin-releasing hormone (TRH) also were examined. Ewes 8-10 days post-estrus were assigned to be treated with: 1) vehicle (n = 5); 2) 0.3 mg domperidone (n = 6); 3) 1.0 mg domperidone (n = 6); 4) 3 micrograms TRH (n = 6); or 5) 10 micrograms TRH (n = 6) every 4 hours for 60 hr. Luteal regression was induced with PGF2 alpha at 12 hr after initiation of treatments. During the luteal phase, pulses of LH were more frequent (P less than .05) and the amplitudes of these were higher (P less than .05) in ewes treated with domperidone or TRH than in control ewes. These changes in LH occurred even though each treatment elevated markedly concentrations of prolactin in plasma. After induction of luteal regression, mean of LH and frequency of LH discharges were similar in all groups. However, in ewes treated with the 1.0 mg/4 hr dose of domperidone the pulse amplitude was greater than in the other groups (2.3 vs 1.1 ng/ml). Dose-response relationships and the magnitude of the prolactin release following domperidone or TRH varied with time. Treatments did not affect the timing of the LH surge or the increase in progesterone associated with the subsequent cycle.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

9.
The objective of this study was to identify rams exhibiting high (HP) and low (LP) levels of sexual performance and to determine whether their respective behavioral responses to ewes in estrus were related to changes in serum testosterone (T) and LH concentrations. Rams were selected on the basis of standardized serving capacity tests. Plasma T and LH concentrations in rams were measured in three experiments: 1) after 15 min of exposure to estrous ewes, 2) after an injection of 500 ng of LHRH, and 3) during an 11-h exposure to estrous ewes. During 15 min of exposure to ewes, HP rams were sexually active, whereas LP rams showed no sexual interest. Secretion of LH was similar (P greater than .05) between ram groups. Sexual arousal, copulation, and ejaculation of HP males were not related (P greater than .05) to LH secretion. Exposure to estrous ewes for 11 h, however, stimulated LH pulse frequency and elevated basal LH and T concentrations in HP but not LP rams (P less than .001). Luteinizing hormone secretion was positively correlated to the frequency of mounts (r = .19; P less than .01) and ejaculation (r = .17; P less than .03). Aggressive behavior of rams directed at ewes was negatively correlated to LH (r = -.22 P less than .003). Concentrations of LH and T after LHRH injection were similar between HP and LP rams (P greater than .05). These results show that the effects of the ewe on LH secretion of rams depend on length of the exposure period and sexual activity of the male.  相似文献   

10.
Endogenous opioid peptides and the control of gonadotrophin secretion   总被引：1，自引：0，他引：1  
The endogenous opioid peptides are a group of recently discovered compounds which occur in the brain of a wide variety of species. Originally named because of their opiate-like activity, they have since been demonstrated to have multifaceted actions, one of which appears to be the modulation of luteinising hormone (LH) secretion. Because of the prime position of LH in the ovulatory process, this role for the opioids has attracted considerable interest. Their mode of action is essentially one of suppression and they work by inhibiting the release of hypothalamic gonadotrophin releasing hormone. Through this mechanism they have been implicated in the suppression of LH secretion during the prepubertal period and the modulation of LH during the oestrous cycle. It is well established that gonadal steroids suppress LH secretion by negative feedback upon the hypothalamic-pituitary axis, and this action may be brought about, in part, through intermediary opioidergic neurones. Much of the research to date has been carried out upon laboratory rodents and primates, but there is evidence now accruing that the opioids have similar actions in domestic animals. Knowledge of the role of these compounds may therefore aid in the understanding of an area of commercial importance, namely the control of ovulation in farm livestock.  相似文献   

11.
This study was designed to evaluate profiles of serum concentrations of LH, pituitary content of LH and GnRH receptors, and hypothalamic content of GnRH in undernourished, ovariectomized ewes. In earlier studies, pulsatile secretion of LH diminished as duration of undernutrition progressed in prepubertal or adult ovariectomized ewes. Ewes having similar body condition scores (CS) of 5 to 9 (1 = extremely thin, 5 = moderate, 9 = obese) were fed maintenance or low-energy diets (100% and 60% of NRC requirements, respectively). Blood samples for analysis of LH were collected at 15-min intervals for 4 h at initiation of the project and immediately prior to slaughter. Serum concentrations of LH did not differ (P greater than .05) among groups at the initial sampling period. At slaughter, ewes with CS less than or equal to 2 (n = 7) had lost 26.8 kg (42% of initial weight). Ewes with CS greater than or equal to 3 (n = 12) had lost an average of 13.7 kg (18% of initial weight). Concentrations of LH in ewes with final CS greater than or equal to 3 was similar (P greater than .05) to that observed during the initial sampling period. However, release of LH was reduced (P less than .01) in ewes with CS less than or equal to 2 compared with ewes with CS greater than or equal to 3 (2.6 vs 9.5 and 3.2 vs 10.5 ng/ml for basal and mean concentrations, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

12.
In earlier in vitro experiments opioids affected steroidogenesis in porcine luteal and granulosa cells. The present studies were undertaken to examine the effects of FK 33-824 (opioid agonist) alone or in combination with LH, PRL or naloxone (NAL, opioid antagonist) on steroidogenesis in cultured porcine theca cells. Moreover, we have tested beta-endorphin-like immunoreactivity (beta-END-LI) concentrations in culture media under control conditions and following treatments of theca cells with LH, PRL, progesterone (P4), oestradiol (E2) or testosterone (T). FK 33-824 and NAL significantly increased P4 release by theca cells and inhibited stimulatory effect of LH on this steroid output. PRL-induced P4 secretion from the cells was blunted only by FK 33-824. Secretion of androstenedione (A4) and T was essentially elevated in the presence of FK 33-824 and this potentiation of both androgen release was completely abolished by PRL. NAL blocked stimulatory effect of the opioid agonist only in case of T. Secretion of oestradiol and oestrone was completely free from the influence of both the opioid agonist and antagonist. Pig theca cells were able to produce beta-END-LI but none of tested hormones (LH, PRL, P4, E2 and T alone or in combination) significantly affected this production. In conclusion, these data indicate that porcine theca cells may produce beta-END-LI and change their steroidogenesis in response to opioid peptides.  相似文献   

13.
Neuropeptide Y (NPY) provides an important hypothalamic link between nutritional status and neuroendocrine mechanisms regulating growth and reproduction. The objective of the following series of experiments was to determine the effects of single or continuous administration of NPY on secretion of luteinizing hormone (LH) and (or) growth hormone (GH). In experiment 1, four ovariectomized (OVX) ewes and four OVX + estrogen-treated ewes each received, in a 4 x 4 Latin Square arrangement of treatments, a single injection of 0, 0.5, 5, or 50 microg NPY via an intracerebroventricular (i.c.v.) cannulae to determine the effects on secretion of GH. NPY significantly elevated serum GH at the 50 microg dose regardless of estrogen exposure (P = 0.003). In experiment 2, eight OVX ewes were infused i.c.v. with NPY or saline (n = 4/trmt) continuously for 20 h in a linearly increasing dose, ending at 50 microg/h NPY. Blood samples were collected via jugular cannulae every 10 min during hour -4-0 (interval 1, pre-treatment), hour 6-10 (interval 2) and hour 16-20 (interval 3) relative to the initiation of infusion (0 h). Mean LH and LH pulse frequency were lower in NPY- versus saline-infused ewes during intervals 2 and 3 (P < 0.01), but NPY had no discernable effect on serum GH (P > 0.10). In experiment 3, four OVX ewes were continuously infused with NPY as in experiment 2, except that the maximum 50 microg/h dose was achieved after only 10 h of infusion. Blood samples were collected every 10 min, beginning 4 h before and continuing until 4h after the NPY infusion. Mean serum LH changed significantly over time (P = 0.0001), decreasing below pre-treatment levels by hour 3 of NPY infusion (P < 0.01), and returning to pre-treatment concentrations following the end of infusion (P > 0.15). Serum GH also changed significantly over time (P < 0.001). Mean GH levels tended to be greater than pre-treatment levels by hour 2 of infusion (P < 0.08), but thereafter returned to basal levels. Serum GH also increased following the end of NPY infusion (P < 0.03). From these data we conclude that NPY exerts a persistent inhibitory effect on secretion of LH, and may stimulate the secretion of GH during the initiation and cessation of infusion of NPY. These observations support a role for NPY in mediating the effects of undernutrition on both LH and GH, and also provide evidence for potential mechanisms by which leptin, acting through NPY, may stimulate the secretion of GH.  相似文献   

14.
The effects of a potent opioid peptide agonist [D-ala2-Phe4, Met(0)ol5-enkephalin (FK 33-824) on the magnitude of the oestradiol-induced LH surge and on basal plasma LH concentrations were examined in intact and chronically-ovariectomized ewes during the late-anoestrous period. In intact ewes, treatment with FK 33-824 (0.5 mg i.v. every 3 hr) for a 24 hr period commencing at the time of oestradiol-17 beta administration (25 micrograms i.m. bolus) was associated with non-significant 65% reduction in the peak plasma LH level observed and a significant (P less than 0.05) 58% reduction in the total amount of LH released during the surge (calculated from the area under the curve). Concurrent treatment with the opioid antagonist naloxone (10 mg i.v. every 3 hr) partially reversed this suppressive effect on the magnitude of the LH-surge. In ovariectomized ewes no significant effects on the oestradiol-induced LH surge of either FK 38-824 alone or FK 33-824 in combination with naloxone were observed. Administration of FK 33-824 at a 6-fold higher dose rate (0.5 mg every 30 min) failed to modify basal plasma LH concentration in intact ewes. In ovariectomized ewes, however, a significant (P less than 0.05) 25% fall in basal plasma LH was observed, an effect which was completely reversed by combined treatment with naloxone (10 mg every 30 min). These results support the conclusion that endogenous opioid peptides may contribute to the neuroendocrine mechanism through which oestradiol promotes a preovulatory-like surge in the anoestrous ewe.  相似文献   

15.
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   

16.
Changes in metabolism of serotonin (5-HT) might mediate the reduced tonic luteinizing hormone (LH) and increased pituitary responsiveness to luteinizing hormone releasing hormone (LHRH) caused by estradiol-17β (estradiol). Two experiments were conducted to determine effects of estradiol, para-chlorophenylalanine (PCPA), an inhibitor of synthesis of 5-HT, and quipazine, an agonist of 5-HT, on tonic and LHRH-induced secretion of LH in ovariectomized ewes during the summer. Tonic levels of LH were reduced, the interval from LHRH to peak of the induced surge was longer and the magnitude of release of LH was greater in ovariectomized ewes treated with estradiol than in controls. Neither PCPA nor quipazine affected tonic secretion of LH. In ovariectomized ewes not receiving estradiol, PCPA and quipazine increased the magnitude of the LHRH-induced release of LH. However, PCPA reduced pituitary sensitivity to LHRH when administered concomitantly with estradiol; treatment with quipazine attenuated this effect of PCPA. The interval to the peak of the induced surge of LH was not affected by PCPA or quipazine in estradiol-treated or control ovariectomized ewes. Based on these results it appears that 5-HT mediates or is required for estradiol to increase pituitary responsiveness to LHRH.  相似文献   

17.
Ketosis is found in various pathophysiological conditions, including diabetes and starvation, that are accompanied by suppression of gonadal activity. The aim of the present study was to determine the role of ketone body in the brain in regulating pulsatile luteinizing hormone (LH) secretion in female rats. Injection of 3-hydroxybutyrate (3HB), a ketone body, into the fourth cerebroventricle (4V) induced suppression of pulsatile LH secretion in a dose-dependent manner in ovariectomized (OVX) rats with an estradiol (E2) implant producing diestrus plasma E2 levels. Plasma glucose and corticosterone levels increased immediately after the 4V 3HB injection, suggesting that the treatment caused a hunger response. The 3HB-induced suppression of LH pulses might be mediated by noradrenergic inputs to the hypothalamic paraventricular nucleus (PVN) because a local injection of α-methyl- p-tyrosine, a catecholamine synthesis inhibitor, into the PVN blocked 3HB-induced suppression of LH pulses and PVN noradrenaline release was increased by 4V 3HB injection in E2-primed OVX rats. These results suggest that ketone body sensed by a central energy sensor in the hindbrain may suppress gonadotropin release via noradrenergic inputs to the PVN under ketosis.  相似文献   

18.
The influence of dietary restriction on the negative feedback potency of 17-beta-estradiol (E2) was evaluated in both castrated male (wethers) and female sheep (OVX ewes) during the breeding season. In study 1, OVX ewes received maintenance or restricted dietary energy for 7 weeks or maintenance energy for 6 weeks prior to a 5 day fast (n=12ewes/feeding group). Estradiol (0.31microg E2/50kg/h) or vehicle (10% EtOH-saline) was continuously infused into half the animals in each dietary treatment for the final 54h of the study. The dynamic pattern of LH secretion was assessed during the final 6h of infusion. Estradiol inhibited luteinizing hormone (LH) pulse amplitude independent of nutrition (P=0.02); fasting increased mean LH, LH peak height, and LH nadir in the absence of E2 (P=0.004, P=0.02, and P=0.02, respectively); while E2 inhibited pulse frequency (P=0.02) and increased peak width (P=0.04) in restricted ewes. Interestingly, despite uniform E2 delivery, serum concentrations of E2 differed with feeding status. Therefore, 12 wethers were infused with 0.31microg E2/50kg/h (6 fed, 6 fasted) and six wethers received 0.19microg E2/50kg/h (fasted) to establish similar serum concentrations of E2 in fed (0.31microg/50kg/h) and fasted (0.19microg/50kg/h) wethers. When fed and fasted wethers had uniform serum concentrations of E2 LH pulse frequency was suppressed (P<0.05) in fasted relative to fed animals, supporting the postulate that energy restriction enhances the E2 negative feedback potency. Collectively, these studies demonstrate that nutrition affects E2 feedback potency and clearance.  相似文献   

19.
Two experiments (Spring and Fall) were conducted in ovariectomized ewes to determine changes in pituitary hormone secretion immediately after pituitary stalk-transection. Ewes underwent either pituitary stalk-transection (SS), sham-transection (SH) or administration of anesthesia only (AO). Stalk-transected, but not sham-operated or anesthetized ewes had polyuria and polydipsia for 7 to 14 days after surgery. Concentrations of luteinizing hormone (LH), follicle stimulating hormone (FSH) and prolactin were measured in peripheral blood samples collected every 10 minutes for a six-hour period. Results were comparable for each season. During the six hours following surgery or removal from anesthesia, concentrations of LH declined in all ewes, but more slowly in SS ewes. No differences in patterns or mean concentrations of FSH were observed. Immediately after surgery, concentrations of prolactin were elevated, then declined in SH and SS ewes. The decrease was greater in SH than SS ewes. Data are consonant with the view that hypothalamic inhibition as well as LHRH stimulation regulate gonadotropin release by the pituitary.  相似文献   

20.
Experiments were conducted to characterize the ability of the antiestrogen enclomiphene (ENC) to block the effects of estradiol on secretion of LH in ovariectomized ewes. To determine whether ENC could block an estradiol-induced LH surge, ewes (n = 4/group) were administered 10 to 250 mg ENC followed 30 min later by 25 micrograms estradiol. Ten or 25 mg ENC suppressed the estradiol-induced LH surge in one of four ewes, whereas 100- or 250-mg doses suppressed the LH surge in three and four of four ewes, respectively. In ewes that received a single treatment of 100 mg ENC plus 25 micrograms estradiol, serum concentrations of LH remained below 1 ng/ml for 3 wk. Compared with untreated ewes, the number of pituitary GnRH receptors was elevated (P less than .05) at 12 d and 28 d, but pituitary content of LH had decreased (P less than .05) by 28 d in ewes treated with 100 mg ENC. To determine whether ENC could block the inhibitory effects of estradiol on serum concentrations of LH, ewes received injections of .03, .1, 1 or 10 mg ENC every 4 d. Half the ewes treated with each dose also received estradiol implants. Injection of .03, .1 or 1 mg ENC alone did not affect serum concentrations of LH, whereas the 10-mg dose decreased serum concentrations of LH below 1 ng/ml by wk 1 of treatment. No dose prevented the inhibition of serum concentrations of LH caused by estradiol implants. In ovariectomized ewes, ENC was antagonistic to estradiol; it prevented the positive effects of estradiol required to induce an LH surge.(ABSTRACT TRUNCATED AT 250 WORDS)  相似文献   

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