Effect of food deprivation on the pulsatile LH release in the cycling and ovariectomized female rat

The effect of food deprivation on the pulsatile release of LH was examined in the normal cycling and the ovariectomized (OVX) adult female rat. In the cycling animals, there were significant decreases in the mean plasma LH levels as well as the frequency and amplitude of the LH pulse 48 h after the onset of food deprivation. On the other hand, food deprivation for up to 72 h did not cause any changes in pulsatile LH release in the OVX animals. No difference in the changes in body weight and blood glucose concentration were found between the cycling and OVX rats throughout the period of food deprivation for up to 96 h. These findings suggest that ovarian factors play an important role in the early manifestation of the effect of food deprivation on pulsatile LH release and that metabolic changes as expressed by decreases in body weight and blood glucose level per se were not the direct causes in the decrease of LH release during the period of food deprivation.     

Effect of administration of an alpha 2-adrenergic agonist, xylazine, on pulsatile gonadotrophin secretion in anoestrous horse mares

Two experiments were performed to test the hypothesis that the seasonal suppression of gonadotrophin pulse frequency in anoestrous horse mares reflects inhibitory neural mechanisms. In a preliminary experiment (Exp. 1) conducted in February, 4 anoestrous mares were sedated by repeated intravenous injections of xylazine, an alpha 2-adrenergic receptor agonist. On the day of treatment, 1-2 LH pulses were observed in xylazine-treated mares. In contrast, during a 12-h period only 1/8 untreated control mares exhibited a LH pulse. In Exp. 2, the effect of xylazine-induced sedation on pulsatile gonadotrophin release was examined in 4 anoestrous mares on two occasions before (18 November and 9 December) and after (23 December and 6 January) an abrupt, artificial increase in day length. Treatment with xylazine was associated with an overall increased FSH (P less than 0.01) and LH (P less than 0.05) pulse frequency, compared with that observed during 12-h pretreatment periods. To evaluate an effect of treatment at the various time during the experimental period, the change in FSH pulse frequency was analysed, since occasionally FSH pulses were unaccompanied by a change in serum LH values indicative of a LH pulse. On two occasions before increased daylength only 1/4 and 3/4 mares exhibited an increase in FSH pulses; in contrast, 14 days after increased daylength (23 December), 4/4 mares exhibited increased FSH pulse frequency associated with treatment. After 27 days of increased daylength (6 January), endogenous FSH pulse frequency was greater than before increased daylength and treatment with xylazine was unaccompanied by a further increase.(ABSTRACT TRUNCATED AT 250 WORDS)     

Seasonal changes in pulsatile luteinizing hormone (LH) secretion in the ewe: relationship of frequency of LH pulses to day length and response to estradiol negative feedback

Seasonal changes in pulsatile luteinizing hormone (LH) secretion in ovariectomized ewes were examined over the course of 2 yr in relation to annual changes in environmental photoperiod, shifts in response to estradiol negative feedback control of LH secretion, and timing of the breeding season. Under natural environmental conditions, the frequency of LH pulses in individual ovariectomized ewes changed gradually and in close association with the annual cycle of day length. As days became shorter in late summer and autumn, LH pulse frequency increased; conversely, as day length increased in late winter and spring, frequency declined. Under artificial conditions in which ovariectomized ewes were exposed to different photoperiods, a similar inverse relationship was observed between day length and LH pulse frequency. The seasonal changes in frequency of LH pulses in ovariectomized ewes, although symmetric with the annual photoperiodic cycle, were not temporally coupled to the dramatic shifts in response to estradiol feedback inhibition of LH secretion at the transitions between breeding season and anestrus. The feedback shifts occurred abruptly and at times when LH pulse frequency in ovariectomized ewes was at, or near, the annual maximum or minimum. The tight coupling between LH pulse frequency and photoperiod leads to the conclusion that there is a photoperiodic drive to the LH pulse-generating system of the ewe. The temporal dissociation between changes in this photoperiodic drive and the seasonal shifts in response to estradiol negative feedback support the hypothesis that the neuroendocrine basis for these two phenomena is not one and the same.     

Seasonal and hormonal control of pulsatile LH secretion in the dairy goat (Capra hircus)

In Exp. 1, the changes in pulsatile LH secretion at the onset of the breeding season were observed in 20 intact, mature Saanen does. Blood was sampled every 20 min for 6 h each week from the beginning of August until the onset of ovulatory activity, as evidenced by cycles in plasma progesterone. The first doe ovulated at the end of August and all were cycling by the end of September. As the first ovulation approached, LH pulse frequency increased by 67% and mean levels of LH increased by 47%. These changes were progressive rather than abrupt. In Exp. 2, seasonal changes in the inhibition of pulsatile LH secretion by ovarian steroids were studied in ovariectomized Saanen does. The animals were untreated (N = 4) or given subcutaneous oestradiol implants (N = 4) and blood was sampled every 10 min for 6 h, twice during the breeding season and twice during the anoestrous season. In each season, the second series of samples was taken after the animals had been treated with progesterone, administered by intravaginal implants. Season did not significantly affect LH secretion in goats not treated with oestradiol, but LH pulse frequency was 54% lower during the anoestrous season than during the breeding season in oestradiol-treated goats. Mean LH concentrations were affected in the same manner as pulse frequency, but pulse amplitude was increased by oestradiol treatment in both seasons. Progesterone had no detectable effect on LH secretion in either season. In Exp. 3, the response to repeated melatonin injections at a set time after dawn was investigated in 11 oestradiol-treated, ovariectomized goats.(ABSTRACT TRUNCATED AT 250 WORDS)     

Orexin-A suppresses the pulsatile secretion of luteinizing hormone via beta-endorphin

Orexins, the novel hypothalamic neuropeptides that stimulate feeding behavior, have been shown to suppress the pulsatile secretion of LH in ovariectomized rats. However, the mechanism of this action is still not clear. We examined the effect of naloxone, a specific opioid antagonist, on the suppression of the pulsatile secretion of LH by orexins to determine whether beta-endorphin is involved in this suppressive effect. We administered orexins intracerebroventricularly and injected naloxone intravenously in ovariectomized rats, and we measured the serum LH concentration to analyze the pulsatile secretion. Administration of orexin-A significantly reduced the mean LH concentration and the pulse frequency, but coadministration of naloxone significantly restored the mean LH concentration and the pulse frequency. Administration of orexin-B also significantly reduced the mean LH concentration and the pulse frequency, and coadministration of naloxone did not restore them. These results indicate that orexin-A, but not orexin-B, suppresses GnRH secretion via beta-endorphin.     

Effect of transport on pulsatile LH release in ovariectomized ewes with or without prior steroid exposure at different times of year

The initial aim of the present study was to test whether the stress of transport suppresses LH pulsatile secretion in ewes. In a pilot experiment in the late breeding season, transport resulted in an unexpected response in three out of five transported, ovariectomized ewes pretreated with oestradiol and progesterone. Before transport, seasonal suppression of LH pulses had occurred earlier than anticipated, but LH pulsatility suddenly restarted for the period of transport. This finding was reminiscent of unexplained results obtained in ovariectomized ewes infused centrally with high doses of corticotrophin-releasing hormone after pretreatment with low doses of oestradiol with or without progesterone. Hence, an additional aim of the present study was to examine whether these latter results with corticotrophin-releasing hormone could be reproduced by increasing endogenous corticotrophin-releasing hormone secretion by transport. Subsequent experiments used groups of at least eight ovariectomized ewes at different times of the year with or without prior exposure to steroids to assess whether these unexpected observations were associated with season or the prevailing endocrine milieu. In the mid-breeding season, transport for 4 h in the absence of steroid pretreatment for 8 months reduced LH pulse frequency from 7.5 +/- 0.3 to 6.3 +/- 0.4 pulses per 4 h (P < 0.05) and LH pulse amplitude from 2.6 +/- 0.5 to 1.8 +/- 0.3 ng ml-1 (P < 0.05). Similarly, in the mid-breeding season, 34 h after the cessation of pretreatment with oestradiol and progesterone, transport suppressed LH pulse frequency from 6.1 +/- 0.4 to 5.5 +/- 0.3 pulses per 4 h (P < 0.05) with a tendency of effect on amplitude (6.2 +/- 2.7 to 2.61 +/- 0.6 ng ml-1; P = 0.07; note the large variance in the pretransport data). During mid-anoestrus, evidence of a suppressive effect of transport was only observed on LH pulse amplitude (4.7 +/- 0.6 versus 3.0 +/- 0.5 pulses per 4 h; P < 0.05) in ovariectomized ewes that had not been exposed to ovarian steroids for 4 months. Repetition of the pilot experiment with 12 ewes during the transition into anoestrus resulted in one ewe with LH pulses seasonally suppressed but increased by transport; 11 ewes had a distinct pulsatile LH pattern which was decreased by transport in six ewes. In anoestrus, there was no effect of transport on LH pulse frequency or amplitude in intact ewes, or those ovariectomized 2-3 weeks previously, with or without prior oestradiol and progesterone treatment. However, basal concentrations of cortisol were greater in anoestrus than in the breeding season, and the increment in cortisol during transport was similar in anoestrus and the breeding season but greater during the transition into anoestrus (P < 0.05). Progesterone concentrations increased from 0.31 +/- 0.02 ng ml-1 before transport to 0.48 +/- 0.05 ng ml-1 during the second hour of transport (P < 0.05). In conclusion, transport reduced LH pulse frequency and amplitude in ovariectomized ewes that had not been exposed to exogenous steroids for at least 4 months. In most animals, the previously observed increase in LH pulsatility induced by exogenous CRH was not reproduced by increasing endogenous CRH secretion by transport. However, in four ewes, transport did increase LH pulsatility, but only during the transition into anoestrus in ewes with seasonally suppressed LH profiles after withdrawal of steroid pretreatment.     

Effects of an opioid antagonist on pulsatile luteinizing hormone secretion in the ewe vary with changes in steroid negative feedback

In ewes during the breeding season, estradiol (E) and progesterone (P) synergistically regulate pulsatile luteinizing hormone (LH) secretion. E primarily inhibits LH pulse amplitude and P inhibits LH pulse frequency. To determine if endogenous opioid peptides (EOP) mediate these negative feedback effects, we administered the long-acting opioid antagonist WIN 44,441-3 (WIN) to intact ewes during the luteal and follicular phases of the estrous cycle and to ovariectomized ewes treated with no steroids, E, P, or E plus P. Steroid levels were maintained at levels seen during the estrous cycle by Silastic implants placed shortly after surgery. WIN increased LH pulse frequency, but not amplitude, in luteal phase ewes. In contrast, during the follicular phase, LH pulse amplitude was increased by WIN and pulse frequency was unchanged. Neither LH pulse frequency nor pulse amplitude was affected by WIN in long-term ovariectomized ewes untreated with steroids. In contrast, WIN slightly increased LH pulse frequency in short-term ovariectomized ewes. WIN also increased LH pulse frequency in ovariectomized ewes treated with P or E plus P. WIN did not affect pulse frequency but did increase LH pulse amplitude in E-treated ewes. These results support the hypothesis that EOP participate in the negative feedback effects of E and P on pulsatile LH secretion during the breeding season and that the inhibitory effects of EOP may persist for some time after ovariectomy.     

Effect of photoperiod on LH, FSH and prolactin patterns in ovariectomized oestradiol-treated heifers

Angus and Angus crossbred heifers were ovariectomized, treated with oestradiol implants and randomly assigned to the natural photoperiod of fall to spring for 43 degrees N latitude or extra light simulating the photoperiod of spring to fall. Weekly blood samples were taken for 6 months (fall to spring equinox). All heifers were cannulated every 4 weeks and blood samples were taken for 4 h at 15-min intervals. Sera were assayed for LH, FSH, prolactin and oestradiol. In samples taken weekly, serum LH and FSH concentrations were higher while serum prolactin was lower in heifers exposed to natural photoperiod. There was a photoperiod X time interaction for both FSH and prolactin with concentrations diverging as photoperiod diverged. Circulating concentrations of oestradiol were not different between groups. In samples taken every 4 weeks at 15-min intervals, baseline concentrations of LH and FSH and LH pulse amplitude were higher while prolactin pulse frequency was lower in heifers exposed to natural photoperiod. There was a photoperiod X time interaction for each of these pulsatile characteristics. The correlation between LH and prolactin concentrations estimated from the 15-min samples differed between the two photoperiod treatment groups. The pooled correlation coefficient (r) was -0.12 under natural photoperiod and +0.50 under extra light. There was also a photoperiod X time interaction with negative correlations occurring when photoperiod was decreasing and positive correlations occurring when photoperiod was increasing. These results support the hypothesis that photoperiod alters serum concentrations of LH, FSH and prolactin in cattle.     

Changes in pulsatile LH secretion after ovariectomy in Ile-de-France ewes in two seasons

Two experiments were conducted in Ile-de-France ewes to study changes in pulsatile LH secretion in ewes ovariectomized during anoestrus or during the midluteal phase of the oestrous cycle. In Exp. 1, blood samples were taken every 20 min for 12 h the day before ovariectomy (Day 0). After ovariectomy, samples were taken every 10 min for 6 h (10 ewes per group), on Days 1, 3, 7 and 15. In Exp. 2 samples were taken every 10 min for 6 h (10 ewes per group) on Days 7, 15, 30, 60, 90, 120, 150 and 180 after ovariectomy. Further samples were taken (5 ewes per group) at 9 and 12 months after ovariectomy. There were significant interactions between season and day of sampling for the interval between LH pulses in both experiments. LH pulse frequency increased within 1 day of ovariectomy and the increase was more rapid during the breeding season. There were clear seasonal differences in pulse frequency in Exp. 2. Compared with ewes ovariectomized in anoestrus, pulse frequency was significantly higher for ewes ovariectomized in the breeding season, from Day 7 until Day 120. Once pulse frequency had increased in ewes about the time of the normal breeding season, pulse frequency remained high and subsequent seasonal changes were greatly reduced. Pulse amplitude increased immediately after ovariectomy to reach a maximum on Day 7 and there were no differences between season of ovariectomy in the initial changes in amplitude. In Exp. 2, changes in amplitude followed changes in pulse interval and there was a significant interaction between season and day of sampling. There were no significant effects of season on nadir LH concentrations which increased throughout the duration of the experiments. These results show that, in ovariectomized ewes, LH pulse frequency observed on a given day depends on time after ovariectomy, season at the time of sampling and on previous exposure of ewes to stimulatory effects of season. The direct effects of season on LH pulse frequency and seasonal changes in sensitivity to steroid feedback may contribute to control of the breeding season and their relative contributions to the beginning and end of the breeding season may differ.     

Does season alter responsiveness of the reproductive neuroendocrine axis to the suppressive actions of cortisol in ovariectomized ewes?

Season can profoundly influence activity of the hypothalamic-pituitary-adrenal axis and alter reproductive neuroendocrine responsiveness to stress and gonadal steroids. Here we tested the hypothesis that the inhibitory effect of a stress-like increment in plasma concentration of the adrenal steroid cortisol on pulsatile LH secretion varies with season. LH pulse patterns were monitored prior to and during the administration of cortisol in the same seven ovariectomized ewes during three stages of the yearly breeding cycle: breeding season, transition to anestrus, and midanestrus. The elevation in cortisol mimicked the rise in plasma level of cortisol in response to an immune/inflammatory stress. During all three seasons, cortisol acutely suppressed the pulsatile release of LH. This inhibition reflected a marked reduction of LH pulse amplitude and a minimal suppression of LH pulse frequency. Of interest, the suppressive effect of this physiologic increment in cortisol did not vary across seasons. This provides initial evidence that, in ovariectomized ewes, cortisol-induced suppression of pulsatile LH secretion differs from that of gonadal steroids in that it is not profoundly influenced by season.     

Superovulatory treatments do not alter pulsatile LH secretion in ovariectomized cattle

Previous work has shown a suppressive effect of superovulatory treatments on pulsatile LH release in cattle. This study tested the hypothesis that this suppression may be caused, at least in part, by a direct effect of commercial gonadotropin preparations on the hypothalamus/pituitary gland. Crossbred Holstein heifers, ovariectomized 20 d before the start of the experiment, received 6 injections of FSH (50 mg Folltropin) at 12-h intervals (n = 6); a single injection of 2500 IU eCG followed by 5 injections of sterile saline at 12-h intervals (n = 6); or 6 injections of saline at 12-h intervals (controls; n = 5). Blood samples were taken every 10 min for 8 h the day before and 3 d after the beginning of treatment to assess LH pulsatility. At the end of these sampling periods, a bolus injection of GnRH (7 ng/kg) was given to assess pituitary responsiveness. There were no effects of the superovulatory drugs on mean LH concentrations, nor on LH pulse frequency or amplitude (P > 0.05). The pituitary response to GnRH was significantly elevated in eCG- but not FSH-treated animals (paired t test; P < 0.05). These data demonstrate that superovulatory preparations do not suppress pulsatile LH secretion independently of the ovaries in cattle.     

FSH and LH concentrations in periparturient mares.

The influence of the ovaries and presence of a foal on periparturient concentrations of FSH and LH were studied in 19 Pony mares. In intact and ovariectomized mares, mean concentrations of FSH fluctuated between 1.1and 9.9 ng/ml on Days -14 to-1 before parturition (Day 0). A surge of FSH occurred in all mares in association with parturition. From Days 1 to 10, the high levels of FSH gradually decreased in the intact group to the minimal concentrations that occur during oestrus, but remained elevated in the ovariectomized mares. There were no significant pre-partum changes in LH in either type of mare. Post-partum changes in LH concentrations increased at a similar rate in ovariectomized and intact mares. The presence of a foal significantly lengthened the interval to first oestrus, depressed LH levels on Days 6--10 and decreased the FSH concentrations as averaged over the 10 days before the first ovulation after parturition.     

Reproductive studies of Brahman cattle II. Luteinizing hormone patterns in ovariectomized Brahman and Hereford cows before and after injection of gonadotropin releasing hormone

Six Brahman and six Hereford long-term ovariectomized cows were bled via tail vessel at 15 minute intervals for a period of 4 hours. Serum was collected and analyzed via radioimmunoassay (RIA) for luteinizing hormone (LH) to determine if ovariectomized Brahman and Hereford cows have pulsatile LH patterns and if breed of animal influenced LH patterns. Brahman and Hereford ovariectomized cattle did have pulsatile LH patterns. Although the trend was for higher LH levels in Hereford than Brahman cows there were no significant differences in mean serum LH levels, number or magnitude of LH peaks or serum LH pulse height.Six Brahman and five Hereford long-term ovariectomized cows were injected (IM) with a single dose of 500μg of gonadotropin releasing hormone (GnRH). Animals were bled via tail vessel at 15 minute intervals for a period of 6 hours. Serum was assayed for LH via RIA to determine if ovariectomized Brahman and Hereford cows differ in GnRH induced LH response. All animals showed increased serum LH in response to GnRH injection within the first 15 minute collection interval. There were no significant differences in duration of response between ovariectomized Brahman or Hereford cows. Ovariectomized Brahman cows had significantly lower (P<.005) Lh values per period than ovariectomized Hereford cows. It was therefore concluded that ovariectomized Brahman cows were significantly less responsive to GnRH induced LH release than were ovariectomized Hereford cows, although duration and shape of the response curves were not different.     

Estrogen and leptin have differential effects on FSH and LH release in female rats

Prior experiments have shown that the adipocyte hormone leptin can advance puberty in mice. We hypothesized that it would also stimulate gonadotrophin secretion in adults. Since the secretion of follicle stimulating hormone (FSH) and luteinizing hormone (LH) is drastically affected by estrogen, we hypothesized that leptin might have different actions dependent on the dose of estrogen. Consequently in these experiments, we tested the effect of injection of leptin into the third cerebral ventricle of ovariectomized animals injected with either the oil diluent, 10 microg or 50 microg of estradiol benzoate 72 hr prior to the experiment. The animals were ovariectomized 3-4 weeks prior to implantation of a cannula into the third ventricle 1 week before the experiments. The day after implantation of an external jugular catheter, blood samples (0. 3 ml) were collected just before and every 10 min for 2 hr after 3V injection of 5 microl of diluent or 10 microg of leptin. Both doses of estradiol benzoate equally decreased plasma LH concentrations and pulse amplitude, but there was a graded decrease in pulse frequency. In contrast, only the 50-microg dose of estradiol benzoate significantly decreased mean plasma FSH concentrations without significantly changing other parameters of FSH release. The number of LH pulses alone and pulses of both hormones together decreased as the dose of estrogen was increased, whereas the number of pulses of FSH alone significantly increased with the higher dose of estradiol benzoate, demonstrating differential control of LH and FSH secretion by estrogen, consistent with alterations in release of luteinizing hormone releasing hormone (LHRH) and the putative FSH-releasing factor (FSHRF), respectively. The effects of intraventricularly injected leptin were drastically altered by increasing doses of estradiol benzoate. There was no significant effect of intraventricular injection of leptin (10 microg) on the various parameters of either FSH or LH secretion in ovariectomized, oil-injected rats, whereas in those injected with 10 microg of estradiol benzoate there was an increase in the first hr in mean plasma concentration, area under the curve, pulse amplitude, and maximum increase of LH above the starting value (Deltamax) on comparison with the results in the diluent-injected animals in which there was no alteration of these parameters during the 2 hr following injection. The pattern of FSH release was opposite to that of LH and had a different time-course. In the diluent-injected animals, probably because of the stress of injection and frequent blood sampling, there was an initial significant decline in plasma FSH at 20 min after injection, followed by a progressive increase with a significant elevation above the control values at 110 and 120 min. In the leptin-injected animals, mean plasma FSH was nearly constant during the entire experiment, coupled with a significant decrease below values in diluent-injected rats, beginning at 30 min after injection and progressing to a maximal difference at 120 min. Area under the curve, pulse amplitude, and Deltamax of FSH was also decreased in the second hour compared to values in diluent-injected rats. In contrast to the stimulatory effects of intraventricular injection of leptin on pulsatile LH release manifest during the first hour after injection, there was a diametrically opposite, delayed significant decrease in pulsatile FSH release. This differential effect of leptin on FSH and LH release was consistent with differential effects of leptin on LHRH and FSHRF release. Finally, the higher dose of E2 (50 microg) suppressed release of both FSH and LH, but there was little effect of leptin under these conditions, the only effect being a slight (P < 0.04) increase in pulse amplitude of LH in this group of rats. The results indicate that the central effects of leptin on gonadotropin release are strongly dependent on plasma estradiol levels. These effects are consistent w     

Orexins, orexigenic hypothalamic neuropeptides, suppress the pulsatile secretion of luteinizing hormone in ovariectomized female rats.

It is well known that feeding disorders are deeply related to reproductive dysfunction, and some feeding regulatory factors may modulate the reproductive function. We examined the effect of orexins, the newly discovered orexigenic hypothalamic neuropeptides, on the pulsatile secretion of LH to clarify their influence on the reproductive function. We administered orexins or saline into the third ventricle of bilaterally ovariectomized (OVX) rats, and measured the serum LH concentration by RIA in blood samples drawn every 6 min for 2 hours to analyze the pulsatile secretion. In the orexin-treated groups, the mean LH concentration and the pulse frequency were significantly reduced (p < 0.01), but the pulse amplitude did not differ significantly. These data indicate that orexins suppress the pulsatile secretion of LH by influencing GnRH neurons at the hypothalamic level.     

Effects of breed, ovarian steroids and season on the pulsatile secretion of LH in ovariectomized ewes

The effects of season and of oestradiol and progesterone on the tonic secretion of LH were studied in ovariectomized Merino and Suffolk ewes, two breeds which differ markedly in the seasonal pattern of their reproductive activity. In the absence of exogenous steroids, the frequency of LH pulses was lower and the amplitude of the pulses was higher in anoestrus than in the breeding season for Merino and Suffolk ewes 30 days after ovariectomy. In long-term (190 days) ovariectomized ewes, this seasonal change in LH secretion was observed in Suffolk ewes only. During seasonal anoestrus, treatment of ewes with subcutaneous oestradiol-17 beta implants (3, 6 or 12 mm in length) decreased the frequency of LH pulses in a dose-dependent manner, with Suffolk ewes being far more sensitive to the inhibitory effects of oestradiol than Merino ewes. The lowest dose of oestradiol (3 mm) had no effect on the secretion of LH in Merino ewes, but reduced secretion in Suffolk ewes. Treatment of ewes with the highest dose of oestradiol (12 mm) completely abolished LH pulses in Suffolk ewes, whereas infrequent pulses remained evident in Merino ewes. During the breeding season, oestradiol alone had no effect on the pulsatile release of LH in either breed, but in combination with progesterone there was a significant reduction in LH pulse frequency. Progesterone effectively decreased LH secretion in both breeds in both seasons. It was concluded that differences between breeds in the 'depth' of anoestrus could be related to differences in the sensitivity of the hypothalamus to both negative feedback by oestradiol and the direct effects of photoperiod.     

Effect of photoperiod on LH, FSH, prolactin and melatonin patterns in ovariectomized prepubertal heifers

Angus and Angus crossbred prepubertal heifers were ovariectomized and randomly assigned to either increasing light simulating the photoperiod of the vernal equinox to the summer solstice (I) or decreasing light simulating the photoperiod of the autumnal equinox to the winter solstice (D) for 43 degrees N latitude. Three blood samples were taken each week for 14 weeks, the first at 11:00 h and two others 2 days later, 1 h before lights on (dark), 1 h before lights off (light). At the end of 14 weeks 4 heifers from each treatment group were cannulated and samples were taken for 12 h at 15-min intervals, 6 h in the light and 6 h in the dark. All sera were assayed for LH, FSH and prolactin. In addition, the samples taken at 15-min intervals were assayed for melatonin. In samples taken weekly at 11:00 h circulating concentrations of LH and prolactin were higher among animals in Group I, while FSH concentrations were not different between Groups D and I. In samples collected weekly in the light or the dark, LH and prolactin concentrations were higher in Group I animals. However, prolactin concentrations were higher and LH concentrations tended to be higher in samples taken in the dark. FSH concentrations were not different between either D or I or dark and light. In samples taken at 15-min intervals the prolactin baseline was higher and pulse amplitude tended to be higher for Group I animals. Neither LH nor FSH pulse characteristics differed between I and D; however, LH baseline and LH pulse amplitude were higher in the dark. Melatonin pulse amplitude was higher among animals in Group D and higher in serum collected in the dark. These results suggest that photoperiod alters circulating concentrations of LH and prolactin and alters pulsatile release of LH, prolactin and melatonin in the prepubertal heifer.     

Release of luteinizing hormone in prepubertal and middle-aged ovariectomized rats

Concentrations of circulating LH were determined in conscious, free-moving ovariectomized rats. All of the animals had been ovariectomized at 24 days of age. Between 30 and 90 days there was an increase in mean blood LH concentrations; a more vigorous pulsatile release of LH characterized by an increase in amplitude and frequency of LH release; and an elevated responsiveness to LHRH administration. Rats which had been ovariectomized for 1 year still had elevated blood LH levels but had episodic pulses of reduced amplitude and a decrease in responsiveness to LHRH. These data suggest that important alterations occur with age in the neuroendocrine mechanisms responsible for the release of LH.     

Opioidergic control of luteinizing hormone release in the female rabbit: influence of ovariectomy and steroid replacement on pulsatile secretion

The influence of ovariectomy and steroid replacement on naloxone-induced changes in pulsatile secretion of luteinizing hormone (LH) in the female rabbit was examined. Blood samples were taken every 5 min through an indwelling catheter in the rabbit ear artery, and plasma was stored until assayed for LH by established radioimmunoassay procedures. In the intact animal, saline injection had no effect on LH secretion. Although naloxone (10 mg/kg) caused a 7-fold increase in mean LH pulse amplitude by 30 min after injection, this increase was not statistically significant because 5 of 11 animals did not respond. In animals ovariectomized 48 h previously, naloxone significantly increased LH concentration by 194% at 23 min after injection. When long-term ovariectomized rabbits were treated with estradiol benzoate and then were given naloxone, no significant increase in LH was observed, although many animals did respond. Treatment of long-term ovariectomized rabbits with 1 microgram estradiol benzoate and 100 micrograms progesterone or 1 mg testosterone propionate on Days 1 and 3 and naloxone on Day 4 resulted in a significant increase in LH 19-24 min later. Although there was an increase in pulse amplitude, no change was detected in pulse frequency after naloxone. These data suggest that the hypothesis of steroid-opioid coupling in the control of LH secretion is not applicable to the female rabbit.     

The effects of short term calf removal on pulsatile LH secretion in the postpartum beef cow

Patterns of secretion of LH were characterized before, during and after 72 h calf separation at approximately 30 days postpartum in nine suckled cows. Calf removal increased both LH concentrations and LH pulse frequency (P<0.01) in the period 48 to 56 h following calf removal in six acyclic cows, but no changes were seen in three cyclic cows. Calf return decreased LH concentrations and LH pulse frequency (P<0.05) within 8 h in the acyclic cows, but no changes were seen in the cyclic cows. Differences in the initial LH parameters and magnitude of the LH responses were apparent between the acyclic cows which responded to calf removal with progesterone secretion and those which did not. These data suggest that suckling inhibits the release of LH acyclic cows and that this is achieved primarily via a reduction in the number of pulsatile releases of LH.