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D H Olster

Publications and source records attributed to D H Olster.

At least 37 records · Page 2Linked to original sources
PubMed1993

Colchicine-induced accumulation of estrogen receptor and progestin receptor immunoreactivity in atypical areas in guinea-pig brain.

Using immunocytochemical techniques, cells containing estrogen and progestin receptors have been observed in many discrete regions of the guinea-pig forebrain, including the mediobasal hypothalamus and preoptic area. While most reaction product is located within cell nuclei, we have reported abundant reaction product in perikaryal cytoplasm and neuronal processes as well. Ultrastructural analysis has revealed the presence of estrogen and progestin receptors in atypical subcellular sites within the hypothalamus, including dendrites and axon terminals. In order to determine if microtubule-dependent intracellular transport is involved in intraneuronal transport of steroid hormone receptors, ovariectomized guinea-pigs were injected intracerebroventricularly with the microtubule inhibitor, colchicine, and brain sections at the level of the hypothalamus were immunostained for estrogen receptors. This treatment resulted in the appearance of estrogen receptor immunoreactivity in the paraventricular and mediodorsal thalamic region, areas typically devoid of estrogen receptor-immunoreactive cells in guinea-pigs. In a second study on progestin receptors, we observed the colchicine-induced accumulation of progestin receptor immunoreactivity in the paraventricular thalamic, mediodorsal thalamic and lateral dorsal thalamic areas as well as in the medial amygdala, all areas typically devoid of progestin receptor immunoreactivity. While estradiol injection induced progestin receptor immunoreactivity in the hypothalamus and preoptic area as described previously, it had no effect on the colchicine-induced accumulation in the thalamus and amygdala. These results provide evidence that in some neurons, progestin receptors and estrogen receptors are transported intracellularly, apparently at a rapid enough rate that they do not ordinarily accumulate within the perikaryon.

Amygdala↗
PubMed1992

Estradiol pulses induce progestin receptors selectively in substance P-immunoreactive neurons in the ventrolateral hypothalamus of female guinea pigs.

Low doses of estradiol, administered as pulses, are as effective as higher doses for priming ovariectomized (OVX) guinea pigs to display progesterone-facilitated lordosis. High doses of estradiol, administered by constant-release implants, induce progestin receptors in many substance P-immunoreactive (SP-IR) neurons in the ventrolateral hypothalamus (VLH), a site at which estradiol primes OVX guinea pigs to respond behaviorally to progesterone. To test the hypothesis that behaviorally effective estradiol pulses induce progestin receptors selectively in substance P-containing neurons in the VLH, OVX females received estradiol implants 1 week prior to perfusion, or two pulses of estradiol-17 beta, injected 39 and 11 h before perfusion. Colchicine was administered intracerebroventricularly prior to perfusion. No significant differences were observed in the total number of progestin receptor-immunoreactive (PR-IR) or substance P-immunoreactive cells in the VLH and VLH/ventromedial hypothalamus (VMH), respectively, of females receiving the two estradiol treatments. However, the percentage of PR-IR cells in the VLH also immunoreactive for SP was significantly higher in the estradiol pulse-treated (53%), than in the estradiol capsule-implanted animals (36%). These data suggest that behaviorally effective estradiol pulses induce progestin receptors selectively in substance P-containing neurons in the VLH and are consistent with the hypothesis that substance P is involved in progesterone-facilitated lordosis in guinea pigs.

Animals↗
PubMed1992

Progestin receptors in substance P-immunoreactive neurons in the hypothalamus of male guinea pigs after behaviorally effective estradiol pulse treatment.

Pulsatile administration of estradiol effectively primes orchidectomized (ORCH) male guinea pigs to display progesterone-facilitated lordosis. In contrast, a single injection of estradiol benzoate (EB) is not behaviorally effective. In ovariectomized female guinea pigs, estradiol pulses induce progestin receptors selectively in substance P neurons in the ventrolateral hypothalamus (VLH), a site at which estradiol primes females to respond behaviorally to progesterone. To test the hypothesis that behaviorally effective estradiol pulses induce progestin receptors selectively in substance P neurons in the VLH in males, ORCH animals received a single injection of EB 40 h before, or two pulses of estradiol-17 beta, 39 and 11 h before perfusion. Colchicine was administered intracerebroventricularly prior to perfusion. The only difference found between the two estradiol treatment groups was a higher number of progestin receptor-immunoreactive (PR-IR) cells in the rostral VLH of estradiol pulse-treated males. There were no significant differences in the number of PR-IR cells in the mid- or caudal VLH, nor in the number of substance P-immunoreactive (SP-IR) neurons in the VLH/ventromedial hypothalamus (VMH) of animals receiving the two estradiol treatments. Furthermore, the percentage of PR-IR cells in the VLH also immunoreactive for SP did not differ between the estradiol pulse- (22%-25%) and the EB-injected animals (22%-32%). These data do not support the hypothesis that administration of behaviorally effective estradiol pulses, as compared to behaviorally ineffective EB injections, induce progestin receptors selectively in substance P neurons in the VLH of male guinea pigs.

Animals↗
PubMed1991

Development of estradiol-induced progestin receptor immunoreactivity in the hypothalamus of female guinea pigs.

The inability of young female guinea pigs to display progesterone-facilitated lordosis has been attributed, in part, to a deficiency in the concentration of hypothalamic estradiol-induced progestin receptors, as measured by in vitro binding assays. An immunocytochemical technique was used to ascertain where, within the mediobasal hypothalamus, estradiol-induced progestin receptor levels are lower in immature than in adult females. Adult (greater than 7 weeks) and juvenile (3 weeks) ovariectomized females received 10 micrograms estradiol benzoate, a dose that primes adult, but not immature females to respond behaviorally to progesterone. Progestin receptor-immunoreactive (PR-IR) cells were counted in the arcuate nucleus (ARC) and ventrolateral hypothalamus (VLH), the two regions containing the densest populations of estradiol-induced progestin receptors in the mediobasal hypothalamus. There was no age difference in the number of PR-IR cells in the rostral or caudal VLH, but immunostaining was darker in the rostral VLH of juveniles as compared to adults. We found similar numbers of PR-IR cells in the rostral and mid-ARC, but 35% fewer immunostained cells in the caudal ARC of immature, as compared to adult females. Furthermore, staining intensity was weaker in the mid- and caudal ARC of the juvenile females. These data suggest that the ARC, not the VLH, is a site of fewer estradiol-induced progestin receptors in immature females.

Aging↗
PubMed1991

Progesterone facilitates lordosis, but not LH release, in estradiol pulse-primed male rats.

Gonadectomized (GDX) male and female rats received repeated cycles of estradiol pulses, which prime animals of both sexes to display progesterone-facilitated lordosis. One, three and six treatment cycles of estradiol pulses followed by progesterone induced progressively higher luteinizing hormone (LH) surges in GDX females. Six treatment cycles of estradiol pulses alone (i.e., without subsequent progesterone treatment) induced a small but significant (approximately 4 ng/ml) increase in LH levels in GDX females. In contrast, GDX males never produced LH surges in response to estradiol pulses alone or estradiol pulses followed by progesterone, regardless of the number of hormone treatment cycles. Thus, female patterns of steroid-induced sexual receptivity and LH release are not inextricably linked, as steroid treatments sufficient for induction of lordosis do not stimulate LH secretion in adult male rats. These data also suggest that the neural system governing the LH surge might be more firmly sexually differentiated than that responsible for sexual receptivity in rats.

Animals↗
PubMed1990

Immunocytochemical colocalization of progestin receptors and beta-endorphin or enkephalin in the hypothalamus of female guinea pigs.

Double-label immunocytochemistry was used to determine whether estradiol-induced progestin receptors and either beta-endorphin or leucine-enkephalin are colocalized in female guinea pig brain. Ovariectomized, adult guinea pigs were implanted with capsules containing estradiol-17 beta to induce high levels of progestin receptors, and injected intracerebroventricularly with colchicine to improve visualization of the opiate peptides. Sections through the hypothalamus and preoptic area were processed for progestin receptor, followed by beta-endorphin or leucine-enkephalin immunocytochemistry. As reported previously, high concentrations of progestin receptor-immunoreactive (PR-IR) cells were found in the preoptic area (medial and periventricular portions, medial preoptic nucleus) and hypothalamus (anterior hypothalamic and arcuate nuclei, ventrolateral area). Many beta-endorphin-IR cells contained PR-IR in the arcuate nucleus and its surroundings (33%) and in the dorsomedial area of the hypothalamus (64%). Scattered enkephalin-IR cells were found in the septal nucleus, medial and lateral preoptic area, bed nucleus of the stria terminalis, and the arcuate nucleus. The ventromedial nucleus of the hypothalamus and dorsolateral magnocellular nucleus, respectively, contained moderate and heavy concentrations of enkephalin-IR cells. Although some of these areas also contained PR-IR, enkephalin-IR was colocalized consistently with PR-IR only in a small number of cells in the arcuate nucleus and ventromedial/ventrolateral area of the hypothalamus. These data, taken together with earlier observations that virtually all cells containing estradiol-induced PR-IR also contain estrogen receptor-IR, provide neuroanatomical evidence that hypothalamic actions of progesterone and estradiol may be mediated by beta-endorphin and/or enkephalin.

Animals↗
PubMed1989

Development of progesterone-facilitated lordosis in female guinea pigs: relationship to neural estrogen and progestin receptors.

Ovariectomized (OVX), 20-day-old female guinea pigs did not exhibit lordosis following treatment with estradiol benzoate (EB) and progesterone. Behavioral responsiveness to EB and progesterone developed abruptly; by 30 days of age, responses typical of adult females (greater than 9 weeks of age) were observed. In vitro assays of neural steroid receptors were performed to test the hypothesis that a deficiency in the concentration of hypothalamic and/or preoptic area estrogen and/or progestin receptors contributes to the lack of progesterone-facilitated lordosis in juvenile (20-day-old) females. Assay of cytosol progestin receptors in the mediobasal hypothalamus (MBH) and preoptic area (POA) of immature and adult females 40 h after injection of EB confirmed a previous report that the concentration of estradiol-induced cytosol progestin receptors in the MBH of juvenile females was slightly lower than that observed in adults. Furthermore, MBH cell nuclear accumulation of progestin receptors after progesterone injection was markedly lower (i.e. 42%) in immature, as compared to adult females. The concentrations of cytosol estrogen receptors in the MBH and POA did not differ between immature and adult OVX guinea pigs. Also, cell nuclear estrogen receptor accumulation in the MBH after estradiol injection was comparable in immature and adult females. These data suggest that a deficiency in cell nuclear progestin receptor accumulation in the MBH may contribute to the absence of progesterone-facilitated lordosis in estradiol-primed, immature female guinea pigs. This age-related difference in cell nuclear progestin receptor accumulation may be due, in part, to reduced concentrations of estradiol-induced cytosol progestin receptors.(ABSTRACT TRUNCATED AT 250 WORDS)

Aging↗
PubMed1989

Development of steroid-induced lordosis in female guinea pigs: effects of different estradiol and progesterone treatments, clonidine, and early weaning.

The ability of developing ovariectomized (OVX) guinea pigs to display lordosis following a variety of steroid treatments which are behaviorally effective in adults was examined. Females OVX at 11 days of age did not display lordosis at 20 days of age, following treatment with several dose combinations of estradiol benzoate (EB, 10-50 micrograms) and progesterone (0.5-5 mg). By 30 days of age, 25% of the animals responded to EB plus progesterone, and by 40 days of age, adult-typical responses were observed. The developmental profile of responsiveness to steroids was not altered by varying the age at OVX, or by allowing pups to remain with a lactating mother. OVX females given estradiol (E2) implants did not exhibit progesterone-facilitated lordosis earlier than those treated with EB: however, the former group did show an unusually high incidence of progesterone-independent lordosis at 40 days of age. Twenty-day-old females also did not respond behaviorally to discrete pulses of E2 followed by progesterone, a treatment which was very effective in adults. Finally, lordosis was not facilitated in EB-primed, 20-day-old females by the alpha-noradrenergic agonist, clonidine, a treatment which was effective in adult females. These data illustrate a variety of conditions under which juvenile female guinea pigs do not exhibit steroid-induced lordosis. Since 20-day-old, EB-treated females also did not exhibit clonidine-facilitated lordosis, incomplete development of the central steroid-responsive and/or noradrenergic systems may contribute to the inability to display steroid-induced estrous behavior at this age.

Animals↗
PubMed1988

Progesterone facilitation of lordosis in male and female Sprague-Dawley rats following priming with estradiol pulses.

Adult male Sprague-Dawley rats rarely exhibit progesterone-facilitated lordosis following steroid treatments which are effective in females. In contrast, progesterone-facilitated lordosis has been observed following priming with estradiol pulses in another strain. The aim of this study was to compare progesterone-facilitated feminine sexual behavior in adult male and female Sprague-Dawley rats following priming with estradiol benzoate (EB) or estradiol pulses. Female sexual behavior was measured in adult, gonadectomized males and females treated as follows: Two pulses of estradiol followed by progesterone or oil the next day; EB (two doses) for 3 days, and progesterone or oil the next day. These protocols were repeated at 4- or 6-day intervals, respectively. Progesterone-facilitated lordosis was observed consistently in both sexes treated with estradiol pulses. By the fifth test, lordosis quotients did not differ between the sexes, but the lordosis ratings in progesterone-treated males remained lower than those observed in females. Proceptivity (hop-darting) was facilitated by progesterone in females, but was never observed in males. Lordosis was induced in both sexes by 15 micrograms EB, but was not reliably facilitated by progesterone. Treatment with the lower dose of EB (1.5 micrograms) induced high levels of receptivity in females (occasionally facilitated by progesterone), but not in males regardless of subsequent treatment (i.e, progesterone or oil). These data suggest that progesterone-facilitated lordosis can be induced in male Sprague-Dawley rats, if a regimen of estradiol pulses is used. Thus, the brain of the adult male is not inflexibly differentiated with regard to progesterone facilitation of feminine receptive behavior.

Animals↗
PubMed1988

Control of gonadotrophin secretion during the pubertal and seasonal transitions in the male sheep.

Castration of spring-born, male Suffolk lambs at 2 weeks of age resulted in a rapid increase in gonadotrophin secretion. LH pulse frequency stabilized by 6 weeks of age and did not change throughout the ensuing summer and autumn. In contrast, LH pulse frequency in castrated, adult rams decreased during the summer and increased in the autumn. Testosterone or oestradiol replacement initially suppressed the post-castration increase in gonadotrophin secretion in developing lambs. Responsiveness to steroid inhibition was lost in late spring and summer (8-15 weeks of age). In steroid-treated castrated mature rams, however, an increase in response to the inhibitory effects of testosterone and oestradiol occurred during the summer, as indicated by slower LH pulse frequencies in June, July and August, than at other times of the year. A decrease in response to inhibition by steroids then occurred in the autumn, months after the springtime reactivation of reproductive function (testicular growth, testosterone and gonadotrophin secretion) in testes-intact adult rams. The results reveal fundamental differences between the regulation of gonadotrophin secretion in ram lambs and adults. The pubertal decrease in response to inhibition by steroids, which is not coincident with a steroid-independent increase in gonadotrophin secretion, may play a key role in increasing gonadotrophin secretion to initiate gonadal activity in the spring. The post-pubertal ram also exhibits the first signs of the seasonal resumption of reproductive activity in the spring. However, it is not until the autumn that a decrease in response to inhibitory feedback by steroids occurs, in concert with a steroid-independent increase in gonadotrophin release. Therefore, in the sexually mature ram, rather than stimulating the initial springtime recovery of gonadal function, these two mechanisms may act in concert to achieve gonadotrophin concentrations and/or patterns necessary to optimize reproductive competence in the autumn.

Animals↗
PubMed1987

Corticotropin-releasing hormone inhibits gonadotropin secretion in the ovariectomized rhesus monkey.

To evaluate whether the compromised gonadotropin secretion frequently occurring during stressful conditions in the primate may be related to an inhibitory action of CRH, the effects of ovine (oCRH) or human (hCRH) CRH on gonadotropin and cortisol secretion were studied in ovariectomized rhesus monkeys. LH secretion (assessed as area under the curve) decreased 35% and 21%, and cortisol increased 37% and 90%, 1-3 h after single iv injections of 200 and 500 micrograms oCRH, respectively (P less than 0.05 vs. pre-CRH control period; n = 4-7/dose). Single injections of 200 and 500 micrograms hCRH, respectively, resulted in 35% and 24% decreases in LH and 40% and 79% increases in cortisol secretion (P less than 0.05). Injections of 100 micrograms oCRH and hCRH elicited significant (P less than 0.05) increases in cortisol release (37% and 31%, respectively), but did not affect LH secretion. A 5-h infusion of hCRH (100 micrograms/h) reduced LH levels (23%, 49%, 59%, 61%, and 62% during the first through the fifth hour, respectively; P less than 0.05 for hours 2-5). FSH secretion also decreased during the hCRH infusion (26%, 33%, 42%, 46%, and 49% during the first through the fifth hour, respectively; P less than 0.05 for hours 3-5), while cortisol increased 76%. These data demonstrate that exogenous CRH administration results in inhibition of LH and FSH secretion in ovariectomized rhesus monkeys. These results are consistent with the hypothesis that elevated CRH levels could contribute to decreased LH and FSH secretion and, thus, disruption of reproduction function under conditions of stress in primates.

Animals↗
PubMed1986

Melatonin and photorefractoriness: loss of response to the melatonin signal leads to seasonal reproductive transitions in the ewe.

Experiments were conducted to examine whether the refractoriness of the Suffolk ewe to the reproductive effects of day length is associated with a deficit in the generation of the circadian rhythm of melatonin secretion or in the postpineal processing of this photoperiodic message. Using serum luteinizing hormone (LH) concentrations in ovariectomized ewes bearing constant-release estradiol implants as a marker of reproductive induction, ewes with intact pineal glands were found to become unresponsive to fixed artificial photoperiods that initially had been either inductive (short days) or inhibitory (long days). The loss of the photoperiodic response was not associated with notable changes in the 24-h secretory pattern of melatonin, which remained characteristically low throughout the day and rose at night. In pinealectomized ewes, nightly infusion of a stimulatory pattern of melatonin (simulating that seen on short days) initially provoked reproductive induction; this response then lessened over much the same time course that pineal intact ewes became refractory to short days. These results support the hypothesis that photorefractoriness reflects a deficit in the postpineal processing of the photoperiodic message. Further, in view of recent evidence that photorefractoriness normally leads to both onset and cessation of the breeding season in Suffolk ewes maintained outdoors, these findings suggest that the loss of response to the melatonin signal contributes to at least one of these reproductive transitions, the cessation of the breeding season, under natural environmental conditions.

Animals↗
PubMed1986

Control of gonadotropin secretion in the male during puberty: a decrease in response to steroid inhibitory feedback in the absence of an increase in steroid-independent drive in the sheep.

The gonadostat hypothesis, i.e. that a decrease in response to the inhibitory feedback action of gonadal steroids occurs during puberty, was tested in the male lamb. Also investigated was whether a simultaneous steroid-independent rise in gonadotropin secretion could be the underlying mechanism for the reduction in steroid feedback sensitivity during puberty. Sexual maturation in intact Suffolk lambs was characterized by increases in all of the following parameters: Serum FSH and LH and LH pulse frequency (during 4-7 weeks of age), testicular size and testosterone (T) concentrations (during 7-28 weeks of age). Estradiol (E2) levels were elevated at 32 weeks. Motile spermatozoa were produced by 16-18 weeks of age. Castration at 5 weeks of age resulted in a prompt increase in gonadotropin concentrations. LH pulse frequency reached a plateau of approximately 5 pulses/4 h (n = 5) at 7 weeks of age and did not change thereafter. T or E2 replacement suppressed pulsatile LH secretion for several weeks. However, despite maintenance of constant serum T (approximately 1.0 ng/ml) or E2 (3-5 pg/ml) concentrations, LH pulse frequency began to increase after 9 weeks of age, and by 13 weeks, pulsatile secretion was apparent in all steroid-replaced castrated lambs. This was well after LH pulse frequency had ceased to increase in untreated castrated animals. These data support the gonadostat hypothesis for puberty in the male lamb. Furthermore, the temporal dissociation of increasing LH secretion in untreated castrated lambs and steroid-replaced castrated lambs suggests that a steroid-independent increase in gonadotropin secretion is not the mechanism underlying the decrease in responsiveness to steroid negative feedback.

Aging↗
PubMed1985

Importance of duration of nocturnal melatonin secretion in determining the reproductive response to inductive photoperiod in the ewe.

The pineal gland, through its nocturnal melatonin secretion, mediates the effects of inhibitory (long) and stimulatory (short) photoperiod on reproduction in female sheep. Earlier studies revealed that duration of the nighttime melatonin rise is important in determining the inhibitory effect of day length on reproduction in the ewe. The present study tested whether the duration is also important in mediating the inductive response to short days. Pinealectomized ewes, housed under long days, received a short-day melatonin infusion (16-h duration) for 90 days. Reproductive status was monitored from the response to estradiol negative feedback of luteinizing hormone (LH) secretion. This short-day melatonin pattern led to unambiguous reproductive induction, despite the exposure to inhibitory long days. The increase in serum LH was comparable, in terms of latency and magnitude, to that in pinealectomized controls receiving the same short-day melatonin pattern under short days, and in pineal-intact controls transferred from long to short days. Since the reproductive status conformed to the length of time that melatonin was elevated each day rather than to photoperiod, these results support the conclusion that duration of the nighttime melatonin rise mediates the reproductive response of the ewe to an inductive photoperiod. In all, the melatonin rhythm is considered an integral component of the physiologic mechanism measuring day length; through duration of its nocturnal secretion, melatonin encodes both inhibitory and stimulatory photoperiods.

Animals↗
PubMed1985

Pineal melatonin mediates photoperiodic control of pulsatile luteinizing hormone secretion in the ewe.

Seasonal breeding in the ewe is regulated by photoperiod through a pineal-dependent mechanism. Changes in the ability of estradiol to inhibit tonic LH secretion are critical. During anestrus, this ovarian steroid gains the ability to slow the frequency of pulsatile LH secretion through an action on the brain. Exposure of ovariectomized, estradiol-implanted ewes to short photoperiods during summer anestrus revealed that daylength can control LH pulse frequency. After removal of estradiol, LH pulse frequency still differed between long- and short-day ewes, suggesting photoperiodic modulation of LH and presumably GnRH secretion independent of gonadal steroids. Significantly, the effects of daylength expressed both in the presence and the absence of estradiol failed to occur in pinealectomized ewes. Long-term infusions of melatonin, given in physiological patterns to pinealectomized ewes, mimicked the effects of photoperiod on pineal-intact ewes. Specifically, a pattern of melatonin characteristic of that in short days (16-hour night-time rise) led to an increase in LH pulse frequency to a breeding season rate. Conversely, melatonin infusions typifying a long-day pattern (8-hour night-time rise) produced an anestrous pulse pattern. Pituitary sensitivity to GnRH was not reduced in sheep which were reproductively suppressed by photoperiod or melatonin treatments. These observations support the conclusion that day-length acts through pineal melatonin secretion to regulate a neural LH pulse generator which, by changing the frequency of GnRH pulses, determines the ewe's seasonal reproductive state.

Animals↗
PubMed1985

Effect of restricted nutrition on puberty in the lamb: patterns of tonic luteinizing hormone (LH) secretion and competency of the LH surge system.

The effects of undernutrition on the timing of puberty and regulation of LH secretion by the inhibitory and stimulatory feedback action of estradiol were examined in female sheep. The first experiment determined that maintenance of low BW (ca., 20 kg, four lambs) between 10 and 45 weeks of age prevented initiation of ovulation at the usual time (30 weeks of age). Ad libitum feeding of such growth-retarded lambs (n = 7) resulted in rapid catch-up growth and onset of reproductive cycles. The second experiment determined the effects of level of nutrition on tonic LH secretion in the presence and absence of inhibitory steroid feedback. Detailed LH patterns were obtained from agonadal lambs (ovariectomy at 20 weeks) that either remained undernourished (ca., 20 kg, 10-39 weeks of age) or were initially undernourished (10-27 weeks) and subsequently fed ad libitum (28-39 weeks). In undernourished lambs (n = 7), LH pulse frequency was slow, and only an occasional LH pulse was detected in the absence of steroid negative feedback; chronic treatment with low levels of estradiol (Silastic capsule), beginning at ovariectomy, prevented pulsatile LH secretion (six lambs). Ad libitum feeding (six lambs) produced a progressive severalfold increase in LH pulse frequency. Estradiol during ad libitum feeding (six lambs) markedly reduced amplitude of LH pulses and retarded the increase in LH pulse frequency. The third experiment, conducted at 40 weeks of age, determined the response to the stimulatory feedback action of estradiol. LH surges were readily induced in undernourished (20 kg) ovariectomized lambs (peak height 51 +/- 16 ng/ml, n = 6 of seven); chronic pretreatment with estradiol markedly reduced the magnitude of the LH surge (peak height 7 +/- 3 ng/ml, four of six). These findings raise the possibility that severe undernutrition prevents ovulation in the lamb by impairing the system governing GnRH secretion and its production of high-frequency LH pulses for follicular development to the preovulatory stage and its establishment of sufficient pituitary LH reserves for release by estradiol stimulatory feedback.

Aging↗