Pattern Of LH Secretion Research Articles

Prepubertal and peripubertal changes in secretory patterns of LH and FSH in beef heifers

Hormonal changes associated with puberty in 14 Norwegian Red×Hereford heifers, born during March to May, were studied in March to June of the following year. Concentrations of LH were determined in plasma samples collected at 20-min intervals for 24 h on four separate days (0, 30, 60 and 75 days after the first collection). These were referred to as prepubertal periods, 1, 2, 3 and 4 in seven heifers which remained prepubertal. In seven heifers which reached puberty during the study, periods were designated as peripubertal (i.e., within 60 days prior to the first rise in progesterone) and luteal or follicular phase. Episodic releases of LH (pulses/24 h) were more frequent during the fourth prepubertal period (9.0 ± 0.8, P < 0.05) than during the first, second or third prepubertal periods or the luteal phase (6.8 ± 0.8, 6.4 ± 0.8, 5.6 ± 0.8 and 5.1 ± 2.1, respectively), but were similar to the peripubertal period (10.7±1.6) and follicular phase (13.8±2.4). Amplitudes of episodic increases in LH were greater during the third prepubertal (5.0 ± 0.4 ng/ml) than during the first, second, or fourth prepubertal period, the peripubertal period or the luteal or follicular phases (3.3 ± 0.4, 3.8 ± 0.4, 3.1 ± 0.4, 2.7 ± 0.4, 1.8 ± 0.5 and 2.3 ± 0.5 ng/ml, respectively). Neither frequency nor amplitude of episodic increases in LH varied between daylight and darkness. There was no evidence of episodic release or of diurnal variation in FSH. Concentrations of estrone were elevated during frequent sampling from catheters compared to single samples collected by venipuncture thrice weekly (9.2 vs. 3.5 pg/ml, P<0.001), whereas concentrations of estradiol averaged 2.0 pg/ml in both types of samples. It is concluded that diurnal variations in LH and FSH are not associated with the maturation process, but increases in either frequency or amplitude of pulses of LH can be detected as heifers mature, depending upon the time before puberty when frequent samples are collected.

Pulse frequency and pulse amplitude of LH are not sufficient to characterize the LH secretory pattern in the normal male

Pulse frequency and pulse amplitude of LH are not sufficient to characterize the LH secretory pattern in the normal male

Characterization of a monoclonal antibody which detects luteinizing hormone from diverse mammalian species

The present study describes the development and characterization of a monoclonal antibody (518B7) generated against bovine LH (bLH). Although 518B7 was extremely specific for LH, very low species specificity was observed. A RIA using this antibody and radioiodinated equine LH (eLH) showed good sensitivity for all mammalian LH preparations tested, with the exception of human LH (15%, relative to the eLH reference standard). Activities of most mammalian LH's ranged between approximately 50–200%. Much less activity was detected with reptilian LH (<1.5%). Amphibian and avian LH fractions were essentially inactive. The reactivities of LH alpha and beta subunits from a variety of mammals clearly showed that the antibody reacts with the beta subunit. Sensitive RIAs were also developed utilizing 125I-bovine and 125I-rat LH. Interestingly, all hormone preparations which showed sufficient reactivity for statistical analysis within the dose ranges used in the present study (0.01–1000 ng/tube) produced a displacement curve parallel to the reference standard. We have also validated the use of 518B7 in detecting LH in serum. Parallel dilution curves relative to purified LH reference standards were observed with equine and bovine serum samples and equine pituitary extract. High (average 94%) recoveries were also seen with bovine serum with known amounts of exogenously added bLH. Similar patterns of LH secretion were detected with a RIA based upon 125I-bLH and 518B7 and a previously described polyclonal antibody-based RIA in bovine serum samples during estrus. Thus, a monoclonal antibody for LH has been produced which can be used to develop sensitive and specific RIAs in many different mammalian species. This antibody can be readily produced in amounts sufficient to provide a stable source of a high quality LH antibody, which may find wide applications in endocrinological research dealing with both domestic and laboratory animals.

Opioid modulation of LH secretion during the oestrous cycle of heifers.

Injections of an opioid agonist (bremazocine) and/or an antagonist (quadazocine) were given to heifers during the luteal or follicular phase of the oestrous cycle. Quadazocine was injected (210 mg/injection) three times at 2-h intervals, and bremazocine was injected (0.45 mg/injection) every 15 min for 6 h. Blood samples were taken every 15 min beginning 6 h before treatments started and continued for 18 h. LH secretion patterns were not affected by quadazocine in the luteal-phase heifers, but quadazocine and bremazocine had marked effects during the follicular phase. Quadazocine increased LH secretion by increasing peak height but not peak frequency. Bremazocine decreased LH secretion through both peak height and frequency. This decrease was of greater magnitude than the increase due to quadazocine. When quadazocine and bremazocine were given together, these effects were cancelled and none of the effects carried over into the bleeding period after treatments stopped. No apparent interruption of follicular maturation was detected since all follicular-phase heifers were detected in oestrus at normal intervals. We conclude that heifers in this experiment did not have an opioid-mediated mechanism for progesterone suppression of LH but that an opioid mechanism for modulating LH does exist during the follicular phase.

Gonadal steroids modulate pulsatile luteinizing hormone secretion by perifused rat anterior pituitary cells.

Recent studies have shown that LH secretion is pulsatile and that LH pulse characteristics are affected by the prevailing steroid environment in both male and female rats. In the present study, a cell perifusion system was used to examine the effects of testosterone (T) and 17 beta-estradiol (E) on LHRH-stimulated pulsatile LH secretion. T inhibited LH secretion, increasing the EC50 for LHRH, while E stimulated secretion, lowering the EC50. Steroid effects were independent of both LHRH pulse amplitude and frequency. E also affected the pattern of LH secretion by facilitating both LHRH self-priming and desensitization to LHRH. These results show that steroids can affect pulsatile LH secretion by actions exerted at the pituitary level and that steroids can induce both quantitative and qualitative changes in LH secretion in the presence of an invariant LHRH stimulus. These results help to elucidate the mechanisms underlying steroid feedback in vivo, since reduction in pituitary responsiveness to LHRH may play an important role in T feedback, while facilitation by E of both self-priming and desensitization may serve to increase the magnitude and shorten the duration of the proestrous LH surge.

Changes in LH pulse frequency and amplitude in intact mares during the transition into the breeding season.

Two groups of mares were exposed to an abrupt, artificial increase or a natural increase in daylength. In both groups, mean LH pulse frequency increased with time of year and was accompanied by a reciprocal decrease in LH pulse amplitude. A non-pulsatile pattern of LH secretion was observed in some mares sampled close to the day of ovulation. Maximum mean LH pulse frequency and the onset of the breeding season occurred earlier in those mares exposed to an abrupt artificial increase in daylength. In blood samples collected frequently, mean serum LH concentrations increased in relation to time of year. However, during 60 days before ovulation, when LH pulse frequency increased, mean daily serum LH values only increased on Day -3 before ovulation. The magnitude of the periovulatory LH rise was greater before the second than the first ovulation of the breeding season. These results support the hypothesis that, in the mare, a photoperiod-induced seasonal alteration in LH pulse frequency and/or amplitude may play a role in the onset of the breeding season.

The female rat as a model describing patterns of pulsatile LH secretion during puberty and their control by melatonin

A characteristic of the advent of final stages of sexual maturation in the rat, the equivalent of puberty in the human, is the development of a specific pattern of pulsatile GnRH secretion, reflected by an equivalent pattern of LH secretion. Many hypotheses have been put forward to explain these last changes, including a change at the hypothalamic level and a modification of the ovary. These models are developed to include melatonin, an indoleamine produced by the pineal gland, which appears to play a role in the establishment of the final pattern of LH secretion, thus affecting both vaginal opening and subsequent estrous cycles. Prior to first ovulation, pulsatile release of LH acquires at least two types of patterns, one with low-amplitude, high-frequency pulses, announcing a pattern observed in the follicular phase of primates, and one with high-amplitude, low-frequency pulses, mimicking what is seen in the luteal phase of primates. From the results presented, it is postulated that chronic melatonin administration increases the number of patterns typical of luteal phases, and reduces those of the follicular type, resulting in a decrease frequency of LH pulses and longer intervals between estrous cycles.

Peptide-steroid interactions in brain regulation of pulsatile gonadotropin secretion

Reproductive function is regulated by an intricate system of peptide, steroid and amine factors interacting within the brain, pituitary and gonads. At no point is the complexity of the reproductive system better exemplified than in the exquisite interplay of factors required to produce and modulate pulsatile gonadotropin secretion. By extension, analysis of the pulsatile secretory pattern of the gonadotropins, as a means of assessing the contribution of these various factors, can reveal interactions too subtle to be detected by the conventional examination of mean gonadotropin concentration. Analysis of the pulsatile secretory patterns of both LH and FSH reveals striking differences between the two gonadotropins in their response to inhibitory, gonadal peptide and steroid factors, suggesting divergent paths of brain-pituitary regulation. Further studies to clarify this disparity in regulation have demonstrated that neutralization of endogenous LHRH completely abolishes pulsatile LH secretion without affecting pulsatile FSH secretion, suggesting the existence of another, as of yet unknown, brain factor which regulates FSH secretion. The feedback signals provided by gonadal steroids can induce both inhibition and facilitation of LHRH and LH secretion. Neurons of the central opiatergic system exert a tonic inhibitory influence on the catecholaminergic neurons regulating LHRH secretion, and are believed to mediate the inhibitory actions of the gonadal steroids on the LHRH system. Withdrawal of the gonadal steroids has been reported to cause a rapid loss of the tonic inhibitory control of the opiate system on LHRH secretion as revealed by a lack of response to naloxone. Reassessment of this system by analyzing the pulsatile pattern of LH secretion, however, reveals that the loss of naloxone effect after gonadectomy occurs very gradually and that an effect can still be obtained up to 2 weeks after the removal of gonadal steroids. These studies provide excellent examples of the complex interplay observed just between selected factors regulating pulsatile gonadotropin secretion. The use of pulsatile gonadotropin analysis is a powerful model, not only for providing greater clarity of known regulatory interactions, but also for revealing new and more subtle levels of control in the brain-pituitary-axis.

Physiological properties of the luteinizing hormone pulse signal: impact of intensive and extended venous sampling paradigms on its characterization in healthy men and women.

The pulsatile nature of the gonadotropin signal is a critical determinant of physiological activation of the gonadal axis. Nonetheless, major uncertainties exist regarding the exact patterns of LH secretion that constitute normal physiological profiles in man. To assess possible bases for the discrepancies in the literature, we sampled blood at 5-min intervals for 24 h in eight normal men and eight normal women in the early follicular phase of the menstrual cycle. The constituent 5-, 10-, 15-, and 20-min immunoactive LH series and the consituent 6-, 12-, or 24-h sampling durations provided ranges of sampling intensities and durations for analysis of significant LH pulses. A technique for minimizing the influence of false positive immunoassay errors on peak detection was used to aid in estimating apparent true positive LH pulse frequency. Nonlinear curve fitting of the relationship between sampling intensity and apparent true positive LH pulse frequency revealed a stable pulse frequency estimate at intensive rates of venous sampling, with values of 19.5 +/- 1.9 (+/- SEM) pulses/24 h (periodicity, 73.8 +/- 6.5 min/pulse) in men and 20.6 +/- 3.6 pulses/24 h (periodicity, 70.0 +/- 10 min/pulse) in women. Further analyses indicated that sampling every 3.1 and 2.0 min for 24 h would be required to capture 90% of the LH pulses in men and women, respectively. Moreover, even with a 5-min sampling rate, the statistical counting errors of the LH pulse frequency estimates varied markedly with sampling duration; for example, in men sampled in 6-, 12-, and 24-hr sessions, the values were, respectively, 49%, 35%, and 24% of the observed pulse frequencies. Similar variations were found in women. Counting errors were 30-50% higher for conventional 20-min sampling rates than for 5-min sampling intervals. Measured interpulse intervals varied widely from 10-330 min (median, 60 min; n = 131 LH pulses) in men and from 10-340 min (median, 65 min; n = 125 LH pulses) in women. In addition, absolute LH pulse amplitudes varied from 1-28 mIU/ml (median, 4.1 mIU/ml) in men and from 1-24 mIU/ml (median, 3.6 mIU/ml) in women. These estimates were associated with a median number of points identified within each pulse of 6.0 in men and 4.0 in women. In summary, the present exhaustive sampling studies demonstrate for the first time stable estimates of physiological LH pulsations in normal men and women, and document broad ranges of normal LH pulse amplitudes and interpulse intervals.(ABSTRACT TRUNCATED AT 400 WORDS)

Modulation of Pulsatile Gonadotropin Secretion by Testosterone in Man

In experimental animals, primary testicular deficiency leads to increased LH pulse frequency. Pulsatile FSH secretion has not been well characterized in any species. To determine the effect of testosterone (T) on the pattern of pulsatile gonadotropin secretion in man, we performed frequent blood-sampling studies in six normal men and six men with primary hypogonadism. All primary hypogonadal men were studied 6-8 weeks after stopping T replacement therapy. Five of the six hypogonadal men were restudied 6-8 weeks after treatment with T enanthate (200 mg, im, every 2 weeks; sampling in this group was 2 weeks after their last T injection). Blood sampling was done at 10-min intervals for 12 h in all subjects, and the pattern of episodic LH and FSH secretion was determined. Normal men had a serum T level of 6.3 +/- 0.3 ng/ml (mean +/- SEM), a LH level of 34 +/- 3 ng/ml, and a LH pulse pattern characterized by low frequency (7.6 +/- 0.7 pulses/12 h) and low amplitude (16 +/- 1 ng/ml). Compared to normal men, primary hypogonadal men had a significantly lower T level (2.9 +/- 0.4 ng/ml) and significantly higher LH pulse frequency (13.0 +/- 1.3 pulses/12 h), amplitude (51 +/- 7 ng/ml), and mean level (222 +/- 26 ng/ml). Reinstitution of T replacement therapy in hypogonadal men resulted in a significant increase in the T level (4.7 +/- 0.5 ng/ml) and significant decreases in LH pulse frequency (7.2 +/- 1.6 pulses/12 h) and amplitude (41 +/- 5 ng/ml) as well as mean LH level (75 +/- 15 ng/ml). FSH levels fluctuated in a distinctly pulsatile pattern in all three groups. Differences in pulsatile FSH secretion between primary hypogonadal men before and during T therapy and normal men paralleled those in pulsatile LH secretion in both frequency and amplitude. These results demonstrate that in man 1) diminished T negative feedback results in high frequency (circhoral), high amplitude LH and FSH pulses; 2) T replacement decreased LH and FSH pulse frequency and amplitude as well as mean levels; and 3) the decreased LH and FSH pulse frequency with T treatment implies that T or a metabolite of T acts on the central nervous system to slow the hypothalamic LHRH pulse generator.

Correlation between LH and estrogen receptor turnover in pituitary and hypothalamus of castrate rats following estrogen agonists and antagonists

A series of studies was undertaken to correlate the short-term dynamics of LH secretion and depletion-replenishment patterns of estrogen receptors (ER) in hypothalamic and pituitary cytosols of ovariectomized rats. Animals castrated for 2 weeks were administered various test compounds and analyzed at 1, 3, 5, 10 and 15h post-treatment. A single injection of 10 βg 17β-estradiol (E 2) to ovariectomized rats elicited α rapid depletion of ER in both pituitary and hypothalamus and a dramatic, though delayed, fall in serum LH. ER replenishment occurred in both tissues through 15h and LH recovered in a similar manner. When cycloheximide was administered along with E 2, ER replenishment was completely inhibited in both tissues; serum LH fell and failed to recover. Actinomycin D injected with E 2 blocked replenishment in pituitary but not hypothalamus; serum LH recovered in parallel with the hypothalamic ER pattern. 17α-E 2 elicited only slight changes in ER and LH was suppressed 10–20% through 15 h. CI-628 caused a near total depletion of pituitary ER with no subsequent replenishment, whereas hypothalamic ER content was virtually unaltered; serum LH was suppressed and later recovered. Orchidectomized rats given 5 μg E 2 demonstrated a less complete ER depletion in hypothalamus, and an earlier replenishment than that seen in pituitary or hypothalamus of similary treated ovariectomized females. Serum LH rebounded to 157% of control levels at 15h. The results indicate that the acute feedback suppression of LH by exposure to estrogens correlates with binding to ER and nuclear translocation. Replenishment and/or retention of cytoplasmic ER in hypothalamus appears to be required for full resumption of LH secretion, following acute suppression.

Pulsatile gonadotropin-releasing hormone treatment in idiopathic delayed puberty.

Idiopathic delayed male puberty is defined as a delay of puberty beyond the age of 16, with prepubertal testosterone levels, normal gonadotropin responses to GnRH (excluding pituitary failure), and normal androgen responses to a single hCG injection (excluding testicular Leydig cell dysfunction), in absence of serious disease. Ten boys with this condition were evaluated as to their spontaneous LH, FSH, and PRL secretory patterns during a 24-h sampling period (20-min intervals). After this all patients were treated with pulsatile infusions of GnRH (25 ng/kg . pulse every 90 min for 10 days. Two groups could be distinguished by means of their pretreatment LH secretory pattern. Five patients had nighttime pulsatile elevation of LH levels, as usually occurs in early puberty. The other five patients did not have such a pattern (prepubertal type). The GnRH treatment resulted in increased LH and testosterone levels in both groups. All patients with pretreatment nighttime pulsatile LH secretion had steady pubertal development during the post-GnRH treatment observation period, whereas the other patients did not. In conclusion, among a number of tests, including chronic pulsatile GnRH treatment for 10 days, only the nocturnal LH secretory pattern differentiated delayed puberty from permanent hypothalamic hypogonadism in boys.

Seasonal variation in the feedback of sex steroid hormones on serum LH concentrations in the male horse.

The possibility of seasonal variation in the feedback effect of testosterone or oestradiol was investigated by giving replacement treatment to geldings for 2-3 weeks during breeding and non-breeding seasons. In the non-breeding season, testosterone suppressed LH values (mean +/- s.e.m., ng/ml) in all geldings (before treatment, 7.5 +/- 2.3; final treatment week, 1.8 +/- 0.2; P less than 0.05), whereas early in the breeding season, testosterone caused a prolonged rise in LH (before, 6.8 +/- 2.3; final week, 18.9 +/- 6.4; P less than 0.05). In all testosterone experiments, LH returned to pretreatment levels within 2 weeks after treatment. Oestradiol treatment caused a prolonged increase (P less than 0.05) in LH concentrations (mean +/- s.e.m., ng/ml) in both seasons (breeding: before 5.2 +/- 1.1; final week, 16.2 +/- 4.8; non-breeding before, 10.9, 20.1 +/- 5.2). We conclude that in geldings the feedback effect of testosterone varies with season and, further, that testosterone replacement may be able to restore to geldings the stallion's seasonal pattern of LH secretion. The results suggest that, in male horses, testosterone and possibly oestradiol, are important components in the neuroendocrine pathway controlling seasonal breeding and, moreover, are essential for the generation of a positive signal for LH secretion in the breeding season.

Pulsatile gonadotropin secretion in women with hypothalamic amenorrhea: evidence that reduced frequency of gonadotropin-releasing hormone secretion is the mechanism of persistent anovulation.

Hypothalamic amenorrhea (HA) is a clinical disorder of unknown etiology. The diagnosis is made by exclusion of known abnormalities of pituitary and ovarian function. To determine if abnormalities of GnRH secretion could account for the anovulation and amenorrhea, we measured plasma gonadotropins every 20 min for 10- to 24-h periods in 19 women with HA. Ovarian steroids and gonadotropin responses to an iv bolus dose of GnRH (25 ng/kg) were also measured. The results were compared to those obtained during the early follicular (EF) and late luteal (LL) phases of ovulatory cycles in normal women. Plasma estradiol was lower (mean +/- SE, 52 +/- 5 pg/ml) than either cycle stage in normal women. Mean plasma LH was lower than EF values and FSH was higher than LL values. The amplitude of LH pulses in HA was similar to that in normal women. LH pulse frequency was the same as that present during the LL, but lower than that during the EF (HA, 4.7 pulses/12 h; EF, 7.7 pulses/12 h; P less than 0.05). In addition to the similar frequency, the patterns of LH secretion in HA resembled that of LL in that the amplitude of LH pulses was highly variable and pulses occurred at irregular intervals. Consistent changes in diurnal gonadotropin secretion were not found, and LH secretion was greater at night in 9 studies and during the day in 5 studies. Repeat studies in three patients (5-13 months later) revealed that LH pulse frequency was variable, being unchanged in 1, increased in 1, and decreased in the third patient. Thus, LH pulse frequency and, by inference, GnRH pulse frequency are similar in HA to those in the normal luteal phase despite a different steroid milieu. GnRH pulse frequency increases from the luteal to the follicular phases of normal cycles and may be important in the initiation of ovarian follicular maturation. These data suggest that the absence of cyclical gonadotropin secretion and anovulation in HA result from a decreased frequency and irregular amplitude of GnRH secretion and consequent absence of ovarian follicular maturation.

Importance of short luteal phases in the endocrine mechanism controlling initiation of estrous cycles in anestrous ewes.

A transient increase in serum progesterone concentrations (to 1 ng/ml for 1-2 days) is observed in the majority of ewes before the first estrous cycle of the breeding season. To determine whether such a brief antecedent rise in progesterone ensures initiation of a full-length cycle by the next LH surge, synthetic GnRH was administered for 3 days to 24 anestrous ewes in a pulsatile fashion designed to mimic the pattern of LH secretion during the preovulatory period of the breeding season. Six ewes received no further treatment, and 6 ewes were treated sc with Silastic implants containing progesterone for 3 days before injecting GnRH. The remaining 12 ewes were treated with additional injections of GnRH every 4 h for the next 5 days. Four of these ewes received a second increase in GnRH pulse frequency, every 2 h and hourly on the subsequent 2 days. An LH surge was stimulated by each regimen of increasing GnRH pulse frequency in all ewes; progesterone pretreatment had no effect on its time of onset, duration, or amplitude. The LH surges induced full-length luteal phases in 10 of 10 ewes when preceded by either an exogenous (n = 6) or an endogenous (n = 4) progesterone increment, but in only 8 of 18 ewes not pretreated with progesterone. These results indicate that a transient increase in progesterone ensures that an ensuing LH surge will initiate an estrous cycle and suggest that progesterone may play an important role in the endocrine mechanisms governing transitions from acyclic to cyclic states.

Internal and external determinants of the timing of puberty in the female.

A working hypothesis is proposed to account for the timing of puberty in female sheep. In the immature female, the frequency of LH pulses is low, and ovarian follicles do not develop to an advanced stage. During the pubertal transition, the frequency of LH pulses increases to drive follicular development and the production of oestradiol which evokes the gonadotrophin surge and ovulation. Central to the hypothesis is the hypothalamic pulse generator for GnRH that directs the pattern and level of LH secretion. Growth-related cues are monitored to regulate the activity of the GnRH pulse generator. When a sufficient body size is attained, the frequency of LH pulses increases both because the sensitivity to oestradiol inhibitory feedback decreases and because the GnRH pulse generator can be accelerated by the steroid. This increase in LH pulse frequency occurs provided the female has experienced the requisite exposure to photoperiod, i.e. the long days of summer followed by the short days of autumn. These photoperiodic cues are transduced by the pineal gland into a humoral signal which is an increased nocturnal production of melatonin. Failure to grow to the appropriate body size or to experience the appropriate exposure to photoperiod leads to a maintenance of the prepubertal anovulatory condition because the GnRH pulse generator operates at low frequency.

Relationships between LH, FSH and prolactin secretion and reproductive activity in the weaned sow

Blood samples were collected from primiparous sows via indwelling jugular cannulae at 15-min intervals for 12 h before and for 24 h (2 sows) or 48 h (10 sows) after weaning and then every 4 h until behavioural oestrus. Weaning to oestrus intervals ranged from 3 to 10 days and 2 sows showed no signs of oestrus and had not ovulated by Days 11 and 16 after weaning. Prolactin concentrations in plasma decreased significantly (P less than 0.001) and reached basal levels 1-2 h after weaning in all sows whilst plasma progesterone concentrations remained basal until approximately 30 h after the preovulatory LH surge in sows that ovulated. Elevated concentrations of prolactin or progesterone during the post-weaning period were, therefore, not responsible for delayed restoration of cyclicity. Overall, mean LH concentrations rose significantly (P less than 0.001) from 0.22 +/- 0.02 during the 12-h period before weaning to 0.38 +/- 0.03 ng/ml during the 12-h post-weaning period. After weaning, pulsatile and basal LH secretions were markedly increased for sows that showed an early return to oestrus (less than or equal to 4 days) compared with sows showing a longer weaning to oestrus interval but a correlation did not exist between either of these LH characteristics and the time taken to resume cyclicity. Mean LH concentrations before weaning were, however, inversely related (r = -0.649; P less than 0.05) to the weaning to oestrus interval. Overall, mean FSH concentrations rose significantly (P less than 0.001) from 151.1 +/- 6.2 (s.e.m.) ng/ml in the 12-h period immediately before weaning to 187.7 +/- 9.7 ng/ml in the subsequent 12-h period but there was no correlation between FSH concentrations, before or after weaning, and the interval from weaning to oestrus. However, a significant correlation was apparent between ovulation rate and peak concentrations of the rise in FSH after weaning (r = 0.746; P less than 0.05) and overall mean FSH values (r = 0.645; P less than 0.05). It is concluded that both LH and FSH concentrations in peripheral blood rose in response to removal of the suckling stimulus at weanling. The increase in LH pulse frequency associated with weaning was not directly related to the weaning to oestrus interval although a specific pattern of LH secretion was observed in sows showing an early return to oestrus (less than or equal to 4 days).(ABSTRACT TRUNCATED AT 400 WORDS)

Lack of influence of mounting on plasma FSH, LH and testosterone concentrations in azoospermic and normospermic young bulls

The influence of mounting and ejaculation on the FSH, LH and testosterone secretory patterns was studied in three azoospermic (including one 61 XXY; one Sertoli-cell-only Syndrome and one secretory-excretory azoospermic) and three control normospermic bulls. Sexual activity did not result in any alteration in the release of these three hormones. There was no difference between the secretory patterns before and after ejaculation in the two classes of bulls. One of the main features was the elevated concentrations of FSH in the bull with Klinefelter's Syndrome, but the mounting test did not result in any significant effect on this concentration. The LH and testosterone patterns were similar for all individuals. From these results, it can be concluded that the mounting test applied under these experimental conditions had no effect on the pituitary-gonadal axis in bulls characterized by either impairment of spermatogenesis or normal semen production.

In vitro simulation of prepubertal changes in pulsatile luteinizing hormone release enhances progesterone and 17 beta-estradiol secretion from immature rat ovaries.

We have previously demonstrated changes in the episodic pattern of LH secretion in female rats as they approach first ovulation. In the present study, ovaries were taken from peripubertal rats and perifused in vitro with a medium containing FSH and LH. The concentration of FSH in the medium was kept constantly low, whereas the concentration of LH was modulated, simulating as closely as possible the various episodic secretory profiles previously observed in vivo. Medium from the perifusion chambers was collected every 10 min for 5 h and assayed for progesterone (P) and 17 beta-estradiol (E2). Exposure of the ovaries to low amplitude LH pulses (20 ng/ml; comparable to those found in the plasma of peripubertal rats during the morning) did not elicit a significant steroidogenic response. On the other hand, exposure to large amplitude LH pulses (80 ng/ml; as seen during the afternoon) led to a marked increase in the output of both P and E2. Similarly, increased steroid secretion occurred when ovaries were exposed to a 2-h minisurge of LH (160 ng/ml) or to a minisurge preceded by three large amplitude pulses (as seen in some animals during the afternoons of the peripubertal period). Continuous exposure to LH at concentrations similar to either the large amplitude pulses or the LH minisurge increased P and E2 release. However, the increase was not significantly larger than that produced by the discontinuous LH perifusion patterns, even though the total amount of LH reaching the ovaries during the 5-h perifusion period was considerably greater. The results show that episodic LH secretion is functionally much more efficient at eliciting release of P and E2 from immature ovaries than is continuous LH secretion. Furthermore, they strongly suggest that changes in the LH secretory pulse patterns, as seen in vivo close to the time of puberty, are fundamental for the activation of ovarian steroidogenesis that leads to the first preovulatory surge of gonadotropins.

The juvenile-peripubertal transition period in the female rat: establishment of a diurnal pattern of pulsatile luteinizing hormone secretion.

Previous descriptions of pulsatile LH release in immature female rats have been mostly inaccurate because of infrequent blood sampling, discontinuous and unbalanced blood replacement procedures, and possibly because of the use of a heterologous RIA. The present study was undertaken to circumvent these problems and to characterize more precisely the changes in episodic LH secretion previously observed during the juvenile-peripubertal transitional period (27-38 days of age). Changes in LH levels were measured in plasma samples obtained every 5 min from unrestrained conscious animals using a recently developed technique that permitted continuous withdrawal of blood for 4-5 h and simultaneous replacement with an artificial blood mixture. In virtually all of the rats, LH release was pulsatile. In both the juvenile (27-29 days old) and peripubertal (30-38 days old) animals, mean plasma LH levels and LH pulse amplitude were low in the mornings. A similar pattern of LH secretion was found in the afternoon during the juvenile period. In contrast, most of the peripubertal animals exhibited an afternoon increase in LH pulse amplitude. A change in pulse frequency was not detected at this time, but a 1.8-fold increase in mean LH levels suggests that large amplitude pulses may be accompanied by low amplitude, high frequency pulses not revealed by the 5-min sampling paradigm. Some of the peripubertal rats (5 of 12) had plasma LH profiles in which the large amplitude pulses were accompanied by a midafternoon minisurge of secretion which lasted for up to 2 h and reached peak levels of 174 +/- 19 ng/ml; the LH surge at first proestrus was greater than 1000 ng/ml. The results demonstrate the prepubertal development of an afternoon increase in LH pulse amplitude and the appearance of a more prolonged and larger secretory episode of LH secretion (minisurge). Disclosure of a concomitant increase in pulse frequency may necessitate blood sampling at more frequent intervals. It is suggested that the changes in the mode of LH release described here may enhance peripubertal ovarian steroidogenesis and provide an appropriate stimulus for initiating the final stages of ovarian development.