Hypothalamic LHRH Content Research Articles

Acute effects of maternal stress on fetal blood catecholamines and hypothalamic LH-RH content.

The acute effects of maternal stress (restraint for 20 to 140 min) on the plasma levels of epinephrine, norepinephrine and dopamine in pregnant rats and their fetuses as well as on the catecholamine content of fetal adrenals and the LH-RH content of fetal hypothalami, were investigated at day 22 of gestation. Despite of a relatively moderate increase of maternal plasma catecholamines a significant increase of norepinephrine (p less than 0.05) and dopamine (p less than 0.05) levels in plasma of the fetuses 30 min after starting maternal stress was observed. The fetal blood concentrations of catecholamines before and during maternal stress were significantly higher than those of the mothers (p less than 0.05 to p less than 0.001). A gradual decrease of the fetal adrenal content of epinephrine and norepinephrine was found, whereas an unchanged content of dopamine of fetal adrenals was registered during maternal restraining. The LH-RH content of fetal hypothalami rose significantly (p less than 0.005) 60 min after starting maternal stress and returned to initial values 140 min after starting restraining.

Effect of Nutritional Stress on the Hypothalamo-Pituitary-Gonadal Axis in the Growing Male Rat

Background/Objective: Nutritional dwarfing (ND) consists of a decrease in weight and height gain and delayed onset of puberty. The aim of the present investigation was to study the modifications induced in male rats by the nutritional stress of a mere 20% reduction in food intake which, however, started immediately after weaning. Materials and Methods: At weaning, male Wistar rats were divided into two groups: Control (C) and ND. C rats were fed ad libitum with a balanced rodent diet. ND received 80% of the diet consumed by C for 4 weeks (T4); then they were fed ad libitum for another 4 (T8) and 8 weeks (T12). The rats were studied at T0, T4, T8 and T12 for the effects of nutritional stress and refeeding on nutritional status, body composition, hypothalamic-pituitary-gonadal axis, and sperm morphology and concentration. Results: ND body weight and length diminished vs. C (p < 0.001). ND body fat percentage decreased 40% (p < 0.001) without change in the percentage of body protein content. The hypothalamic content of LHRH did not change. However, FSH, LH and testosterone serum levels had significantly decreased (p < 0.001) at T4 in ND rats. A 48.4 % decrease in serum leptin in the ND group was observed at T4 (p < 0.05). The absolute testicular and seminal vesicle weight was significantly decreased by ND at T4 (p < 0.001). At T4 the percentage of anomalies of caudal spermatozoa increased in about 64% (p < 0.001) of ND vs. C rats, despite the unchanged sperm concentrations. All parameters normalized during refeeding. Conclusion: In this model, a decrease in leptin due to nutritional stress could be responsible, at least in part, for the inhibition of reproductive function. Refeeding normalized all parameters studied.

Effects of Superior Cervical Ganglionectomy and Melatonin Replacement on Intra-hypothalamic LHRH Content and Pulsatile Luteinizing Hormone Release in the Mink

Long-term effects of subcutaneous melatonin implants on intrahypothalamic LHRH content and on pulsatile luteinizing hormone release have been investigated in ganglionectomized male mink. Animals were submitted to bilateral removal of the superior cervical ganglion in mid-April. A preliminary study revealed that plasma LH concentrations remain at a basal level throughout the year following ganglionectomy. In a second experiment, one month after ganglionectomy and transfer from the natural photoperiod environment to short daylengths (LD 4:20), melatonin pellets were subcutaneously implanted to overcome deafferentation of the pineal. Progressive effects of treatment were studied 7 days, 15 days, and one, two and three months after insertion of the melatonin implants. The intra-hypothalamic LHRH content in ganglionectomized mink was at a basal level similar to that observed during seasonally sexual quiescence, or after exposure to inhibitory long days (LD 20:4). A significant and transient elevation in LHRH content was observed already after fifteen days, and also one month after insertion of melatonin implants. This resulted in mean values similar to those observed during the breeding season, or after exposure to stimulatory short days (LD 4:20). A decrease in hypothalamic LHRH content started after two months. No pattern of pulsatile LH secretion was recorded in ganglionectomized untreated mink. A significant increase in all parameters of pulsatile LH secretion was observed fifteen days after the elevation of LHRH content induced by melatonin treatment, and maximum values were reached after two months. Pituitary activity tended to decrease after three months, characterized in particular by a significant decrease in the mean frequency of LH pulses. In addition, the increase in pulsatile characteristics of LH release occurred two months before the peripheral renewal of testicular activity. Apparently, the reproductive endocrine function in ganglionectomized mink treated with melatonin implants is restored more rapidly at the hypothalamic level than at the pituitary or testicular levels.

Mechanisms of altered LH secretion in neonatally oestrogenized male rats

It is well known that the control of LH secretion depends on the steroid milieu during the postnatal period. In this study LH secretion was analysed in adult male rats injected neonatally with 500 micrograms oestradiol benzoate (1) after orchidectomy, (2) after selective elimination of androgens by destruction of Leydig cells with ethylene dimethane sulphonate (EDS), and (3) after removal in orchidectomized animals of Silastic capsules containing testosterone. In addition, (4) in vivo and in vitro LH secretion in response to LHRH agonist and antagonists, (5) the hypothalamic LHRH content, (6) the basal and stimulated in vitro LHRH release, and (7) the LH responses after administration of naloxone (2 mg/kg), alpha-methyl-p-tyrosine (alpha-MPT; 250 mg/kg), N-methyl-D-aspartic acid (NMDA, 15 mg/kg) or kainic acid (KA; 15 mg/kg) were also examined. Our data indicated that (1) the LH response after orchidectomy, after EDS administration and after removal of Silastic capsules containing testosterone was diminished in oestrogenized male rats, (2) the pituitaries from oestrogenized males retained responsiveness to LHRH, (3) hypothalamic LHRH content was reduced in oestrogenized males, but the hypothalamus from oestrogenized males released more LHRH than those of control groups both under basal conditions or after depolarization, (4) alpha-MPT decreased LH secretion only in oestrogenized males, and (5) NMDA and KA stimulated LH only in oestrogenized males. We conclude that in oestrogenized male rates the loss of sensitivity to the negative feedback action of testosterone on LH secretion was not due to decreased pituitary responsiveness to LHRH stimulation or to the inherent damage of LHRH neurones.(ABSTRACT TRUNCATED AT 250 WORDS)

Repeated intracerebroventricular administration of taurine lowers LH levels and postpones vaginal opening in peripubertal female rats

We investigated the effect of repeated intracerebroventricular injections of taurine (Tau, 0.15 μ mol/3 μl distilled water), administered during postnatal days 23–29, on serum LH levels, and on the hypothalamic content of LHRH and amino acid neurotransmitters (measured by HPLC and electrochemical detection) in 30-day-old female rats ( n = 18). Treatment with Tau lowered serum LH (Tau: 0.20 ± 0.04; Controls: 1.04 ± 0.21 ng/ml RP3; mean ± S.E.M.; P < 0.05) as well as hypothalamic LHRH levels (Tau: 82.6 ± 9.5; Controls: 128.7 ± 14.1 pg/mg wet tissue, P < 0.05). Tau treatment doubled hypothalamic GABA levels (Tau: 31.3 ± 2.9; Controls: 15.6 ± 1,2 nmoles/mg wet tissue, P < 0.001). In a second group of animals ( n = 13), Tau treatment delayed vaginal opening by more than 2 days ( P < 0.05 vs. controls). It is concluded that supplementation with Tau during the fourth postnatal week reduces LHRH/LH secretion and postpones sexual development, perhaps by increasing the activity of the hypothalamic GABAergic system.

Hormonal Pattern of the Pheromonal Restoration of Cyclic Activity in Aging Irregularly Cycling and Persistent-Estrus Female Rats1

This study reports the hormonal pattern of pheromonal restoration of cyclic activity (PRCA) in irregularly cycling (IC) and in anovulatory persistent-estrus (PE) aging female middle-aged Wistar rats. Hypothalamic content of LHRH and plasma levels of LH, FSH, estradiol (E2), and progesterone (P) were measured by RIA methods, and prolactin (PRL) was examined by ELISA in 1) normal four-day cycling rats, 2) saline-treated IC and PE rats, and 3) IC and PE rats treated with sprays of male urine (50 microliters every 10 min for 1 h on only one day, at a distance of 1 cm from the nostrils). Group 1 showed low levels of LHRH and high levels of LH, FSH, E2, P, and PRL in the afternoon of proestrus (PR). In group 2, the pattern was not cyclical and the levels of the hormones were higher than basal for the cyclic rats, except for P, which was lower. Group 3 showed a depletion of the hypothalamic LHRH and an increase in plasma LH, FSH, E2, Pm, and PRL. FSH, E2, and P showed the strongest rise, leading to an elevated ratio of FSH to LH. Four-day estrous cycles reappeared in urine-treated rats on the succeeding days. The cyclic behavior of the PRCA hormones was, qualitatively, the same as in the normally cycling rats. According to the results, the origin of the PRCA effect is an olfactory input to the hypophysiotropic area of the hypothalamus.(ABSTRACT TRUNCATED AT 250 WORDS)

Alterations in hypothalamic and pituitary hormone levels induced by neonatal treatment of female mice with diethylstilbestrol

Neonatal female mice of the NMRI strain were treated with the synthetic estrogen diethylstilbestrol (DES), 5 μg daily for the first 5 days after birth, or with vehicle only. Levels of LH and FSH (pituitary and serum) and LHRH (hypothalamus) were measured by radioimmunoassay (RIA) in 6- to 56-day-old females with 6- to 7-day intervals. Compared to controls, DES-treated females had low levels of LH on days 6, 12, and 21 in the pituitary, and on days 6 and 12 in serum; increased LH levels were seen in both the pituitary and serum on day 42. The FSH levels of DES-treated females were decreased on days 6 and 12 in the pituitary and on day 6 in serum; an increased FSH content occurred on day 21 in the pituitary. In the preoptic area and basal hypothalamus of DES-treated females, levels of LHRH were increased on day 21 and decreased on day 42. On day 56, the serum levels of FSH and LH and the hypothalamic content of LHRH were similar in controls and DES females. A second study including both synthetic and natural estrogen was performed in 12-day-old females. Treatment with 10 −2 μg DES or lower doses or 5 μg estradiol-17β (E 2) on days 1 to 5 after birth had no depressive effect on serum LH. The hypothalamic-pituitary-ovarian feedback system reacted similarly to ovariectomy and E 2 challenge in 15-day-old control and DES-treated females. DES-treated 56-day-old females had a reduced LH response to ovariectomy but increased response to exogenous E 2 compared to controls. These results show that neonatal treatment with DES has pronounced effects on the hypothalamic-pituitary system in the developing female mouse, which may be of importance for the altered ovarian function in these females as adults.

Influence of photoperiod and 6-methoxybenzoxazolinone on the reproductive axis of inbred LSH/Ss Lak male hamsters

Adult male Syrian hamsters of the inbred LSH/Ss Lak strain were maintained under a 14L:10D light cycle until 13 weeks of age. At this point, they were implanted s.c. with elastomer capsules that were either empty or packed with 30-40 mg of 6-methoxybenzoxazolinone (6-MBOA), a compound found naturally in some monocotyledonous plants; half of the animals from each treatment group were then kept in long days (14L:10D) or transferred to short days (9L:15D). Testicular size was measured and blood samples collected from each hamster immediately before capsule implantation and again 2, 4, 6 and 8 weeks later. Within just 2 weeks of exposure to short days the mean plasma levels of LH and FSH had significantly declined, in both the control and 6-MBOA-treated animals, and were basal within 4 weeks. Testicular size closely followed these gonadotrophin changes; within 4-6 weeks the testes from all of the short-day hamsters had completely regressed to a prepubertal size. At the end of the experiment, at Week 8, the animals were killed and various components of the hypothalamo-pituitary-testicular axis were compared between the treatment groups. The pituitary content of FSH and LH, testicular weight, mean serum level of testosterone, but not hypothalamic LHRH content or pituitary gland weight, were considerably lower in the short-day than in the long-day hamsters, regardless of whether or not they had been chronically treated with 6-MBOA.(ABSTRACT TRUNCATED AT 250 WORDS)

Analysis of the hypothalamic-pituitary-ovary axis in the neonatally-androgenized female rat

The administration of testosterone propionate (TP) in the female rat at the neonatal age has been used for several yr as a model to study anovulation during adulthood. The present work was designed in order to see whether some neuroendocrine parameters vary with age in this animal model. Hypothalamic LHRH content and LH-FSH anterior pituitary (AP) content and plasma levels were evaluated in samples taken from both neonatally-androgenized and littermate control female rats at different ages (15 to 100 days old). Additionally, we have studied pulsatile LH-FSH released in plasma and in vivo AP response to LHRH in both neonatally-androgenized and control female rats during adulthood. The results indicate that the neonatal TP treatment did not induce any change in hypothalamic LHRH content over development. Neonatally androgenized rats have decreased both LH-FSH AP content and plasma levels at the infantile age (15-day old). LH-FSH AP content remained reduced in samples taken up to the 30th day of age. Plasma LH-FSH levels on the day 30 of age were similar in both groups. TP-treated rats studied on the 100th day of age had: a) an altered pulsatile rhythm of gonadotropin release in plasma due to the decreased LH-FSH trough and average mean values, and to the diminished FSH peak amplitude values, as well as an increased LH:FSH ratio; and b) an impaired in vivo LHRH-induced LH-FSH release.(ABSTRACT TRUNCATED AT 250 WORDS)

Role of LHRH in the gonadotrophin response to restraint stress in intact male rats

A hypothalamic site of action has been hypothesized for the inhibitory effect of chronic stress on gonadotrophin secretion. The aim of the present study was to examine the temporal changes in hypothalamic LHRH content and gonadotrophin secretion during restraint stress, and the pituitary responsiveness to LHRH stimulation in chronically stressed rats. Adult male rats were killed after being restrained for 0, 20, 45, 90, 180 and 360 min or for 6 h daily over 2, 3 and 4 days. After 20-45 min of stress there was an increase in plasma concentrations of LH (P less than 0.01) and a decrease in hypothalamic LHRH content (P less than 0.01), suggesting a negative correlation between plasma LH and hypothalamic LHRH concentrations. Plasma concentrations of FSH were also increased by restraint, but the FSH response was slower and less than the plasma LH response, being significant after 90 min of restraint. Plasma LH and FSH and hypothalamic LHRH concentrations were decreased in chronically stressed rats. In rats restrained for 6 h daily over 4 days, the response of plasma gonadotrophins to administration of 500 ng LHRH was enhanced 45 min after the injection. On the basis of these observations we concluded that in the intact rat, stress may acutely stimulate LHRH and gonadotrophin secretion, and the inhibitory effect of chronic stress on plasma LH and FSH seems not to be due to a reduction in pituitary responsiveness to LHRH, but rather to a decrease in LHRH secretion.

Photoperiodic control of the development of the LHRH neurosecretory system of European starlings (Sturnus vulgaris) during puberty and the onset of photorefractoriness.

The development of the reproductive system was studied in juvenile starlings during the acquisition of photosensitivity, the attainment of sexual maturation after photostimulation and the subsequent onset of photorefractoriness, using immunohistochemistry for LHRH and radioimmunoassay measurements of hypothalamic, pituitary and plasma hormone concentrations. The first stage of sexual development induced by exposure of photorefractory immature starlings to short days (8 h light:16 h darkness; 8L:16D) was characterized by a decrease in pituitary prolactin content within 1 week and an increase in hypothalamic LHRH content, in the size of the LHRH perikarya and in the intensity of immunostaining in the median eminence in 4-6 weeks. Sexual maturation occurring after exposure to long days (18L:6D) was associated with further increases in LHRH content and cell size, and increases in LH and prolactin concentrations. During testicular regression, LHRH perikarya were reduced in size and staining intensity but LHRH immunostaining in the median eminence and content in the hypothalamus remained high until gonadal regression was almost complete. Prolactin levels were maximal during testicular regression. These results suggest that gonadal regression is initiated by a reduction in LHRH synthesis and possibly, in addition, an external inhibitory influence on LHRH release. Hypothalamic LHRH content eventually declined and LHRH immunostaining in the median eminence was much reduced in fully photorefractory starlings maintained under long days.

Effect of Neonatal Androgenization on the Testosterone Feedback Sensitivity in Adult Rats in Two Lighting Conditions

Neonatally androgenized and intact adult male Wistar rats received daily, during 1 week, either testosterone propionate or sesame oil injections in periodic or constant light. Serum and pituitary gonadotropins and hypothalamic LHRH were measured. In periodic light, neonatal androgenization did not change the serum concentration or pituitary contents of gonadotropins, or the hypothalamic content of LHRH. Testosterone injections decreased serum concentration and pituitary content of gonadotropin of intact rats but failed to decrease the pituitary gonadotropin content of neonatally androgenized rats. In constant light, serum FSH was decreased in neonatally androgenized rats. Testosterone injections decreased both serum LH and FSH concentrations of intact rats but only serum LH of androgenized rats. Pituitary gonadotropin and hypothalamic LHRH contents remained unchanged. We conclude that neonatal androgenization renders the male rat hypothalamo-pituitary axis more resistant to changes of testosterone concentration in adulthood. Constant light did not sensitize the neonatally androgenized rats to testosterone, but on the contrary, testosterone injections were less effective in constant than in periodical light.

LHRH and LH in peripubertal female rats following prenatal and/or postnatal ethanol exposure

The effects of pre- and postnatal exposure to ethanol (ETOH) on LHRH and LH were investigated. Pregnant and/or lactating dams were fed ETOH during: 1) gestation, 2) lactation, or 3) gestation-lactation. Female offspring were decapitated at 30 or 40 days-of-age; trunk blood was collected for plasma LH RIA; and hypothalamic tissues were collected for LHRH RIA. Hypothalamic LHRH content of all ETOH-exposed groups was less than that of non-ETOH-fed controls at 30 and 40 days-of-age (p<0.05). Plasma LH concentrations of all ETOH-exposed groups were less than those of non-ETOH-fed controls at 30 and 40 days-of-age (p<0.05). Also, at 30 and 40 days-of-age, the plasma LH concentrations of the animals exposed to ETOH during lactation and gestation-lactation were less than those of the animals exposed to ETOH during gestation (p<0.05). These data suggest that ETOH exposure during gestation and/or lactation negatively affects hypothalamic LHRH content of female rat offspring. Decreased hypothalamic LHRH content with corresponding lowered plasma LH concentration suggests that ETOH influences development or maturation of hypothalamic LHRH neurons by possibly decreasing their number or synthesizing capability.

Immunoreactive LHRH in chronic starved rats.

The effects of chronic starvation (1/4 of ad libitum food intake) for 21 or 30 days were studied on the hypothalamic and serum concentrations of LHRH, the pituitary and serum concentrations of LH, and the weights of the anterior pituitary, ovary and uterus in adult female Wistar rats (chronic starved group, CSG). Control female rats were fed ad lib. for the same periods (control group, CG). On day 22 or 31, half of the rats of each group were weighed and sacrificed by decapitation. Since there were no difference on above parameters between the experiments on 22nd and 31st day, the results were combined for each parameters. At the time of sacrifice, the body weight of CSG was on the average 44% lower than that of CG rats, and also marked reduction in anterior pituitary (44%), ovarian (61%) and uterine weights (69%) was observed. Serum LH concentrations (mean +/- SE; 5.67 +/- 0.67 versus 33.30 +/- 6.00 ng/ml, P less than 0.001) and pituitary LH content (286.7 +/- 19.4 vs 451.0 +/- 32.8 micrograms, P less than 0.001) were significantly decreased in CSG than in CG rats. However, pituitary LH concentration was not reduced because of the proportional reduction to the pituitary weight of CSG rats. Hypothalamic immunoreactive LHRH (IR-LHRH) content in CSG showed a significant increase as compared to CG rats (5.77 +/- 0.52 vs 4.41 +/- 0.27 ng/hypothalamic extract, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Positive and negative feedback regulation of plasma LH by sex steroids and hypothalamic LHRH content in neonatally estrogenized female rats

Positive and negative feedback regulation of plasma LH by sex steroids and hypothalamic LHRH content in neonatally estrogenized female rats

Interactions of testosterone and short-photoperiod exposure on the neuroendocrine axis of the male Syrian hamster.

Exposure of adult male golden hamsters to short days (less than 12.5 h light/day) leads to suppression of gonadal function which is secondary to reductions in gonadotropin and prolactin (PRL) secretion. Short-day (SD) exposure also leads to a reduction in hypothalamic norepinephrine (NE) and dopamine (DA) metabolism and an increase in hypothalamic LHRH content which appears to be related to a decrease in LHRH release. To determine whether SD-induced changes in NE and DA metabolism are dependent or independent of changes in circulating testosterone (T) levels and thus possible mediators of photoperiod effects on gonadotropin secretion, the effects of castration and steroid replacement on hypothalamic amine metabolism were studied in male hamsters maintained under long or short photoperiod conditions. The presence of Silastic T-implants resulted in a greater suppression of LH and FSH in SD than in long-day (LD) hamster, but increased median eminence (ME) LHRH content in both groups. Exposure of castrate hamsters to short days led to a reduction of NE turnover in the ME and medial preoptic-suprachiasmatic area (MPOA) and a decrease in serum FSH levels. LH levels tended to be lower, but not significantly so. The decrease in ME NE turnover was potentiated by T replacement, but in the MPOA-SCN, T-implants reversed the effects of short days. NE turnover in the MBH was reduced by T in both LD and SD animals, but the effect was much greater in the SD animals. SD exposure also caused a decrease in ME DA metabolism that was reversed by T replacement.(ABSTRACT TRUNCATED AT 250 WORDS)

Opioid modulation of LHRH release in vitro depends upon levels of testosterone in vivo.

The in vitro release of LHRH from hypothalami of adult male rats (intact, 5-day castrates, 5-day castrates replaced with various doses of testosterone) was measured under basal conditions and after the addition of KCl, the opiate antagonist naloxone or the opiate agonist DAGO to the perifusion medium. Hypothalami from all treatment groups responded to 56 mM KCl with an increased output of LHRH. LHRH release was also induced by naloxone (10(-6)M), but only from tissues derived from intacts and castrates given physiological doses of testosterone. The opiate agonist DAGO (10(-6)M) did not alter the basal release of LHRH; it, however, caused a significant decrease in the K+-induced release of LHRH from hypothalami derived from intact rats and rats replaced with physiological levels of testosterone but not from those derived from castrate rats or castrate rats replaced with small amounts of testosterone. The specificity of this latter response was shown by its reversibility with naloxone. The lack of DAGO effects upon tissues from rats with low levels of steroid implied steroid dependency of the response to opioidergic influences and indeed, the response to DAGO was restored when testosterone was replaced at physiological doses. Measurement of hypothalamic LHRH content showed no significant differences between tissues obtained from intact, castrate and testosterone-replaced castrate rats. These in vitro data support the view that the inhibitory influence of opioids upon LHRH release depends on the presence of gonadal steroids in vivo.

Hypothalamic-pituitary function in experimental uremic hypogonadism.

In companion studies we have shown that chronic uremic male rats are infertile and hypoandrogenic and have lowered basal LH levels. Fertility was restored by either human CG (hCG) or testosterone treatment. Testicular steroidogenic responses to hCG in vivo and in vitro were normal or excessive, indicating that hypothalamic-pituitary dysfunction was the predominant early lesion in uremic hypogonadism. Further studies were undertaken to characterize the nature of the central defects in regulation of pituitary LH secretion. Uremic rats have reduced MCRs for rat LH (rLH) (61%), rat FSH (rFSH) (47%), and LHRH (41%). Pituitary gonadotropin and hypothalamic LHRH content were unchanged in uremic rats. Pituitary rLH and rFSH responses to LHRH stimulation in vivo and in vitro were quantitatively normal or excessive, with delayed peaks suggesting that uremic pituitary gonadotrope secretion is deficient due to lack of appropriate hypothalamic LHRH drive rather than intrinsic pituitary defects. Despite reduced pituitary gonadotropin secretion in intact uremic rats, castration induced paradoxical excessive increases in pituitary LHRH binding, serum rLH, and rFSH beyond those of nonuremic controls. Paradoxical postcastration hyperresponses of serum rLH and rFSH were not due to circulating immunoreactive fragments of gonadotropins or undernutrition. Dysfunction of the uremic hypothalamus was further characterized in vivo by lack of rLH responsiveness to naloxone and hypersensitivity to negative testicular feedback in castrate-steroid-replaced and intact rats. These data demonstrate that uremic hypogonadism is principally due to aberrant hypothalamic regulation of pituitary LH secretion resembling those of the immature rat or seasonally regressed animal. This recrudescence of the inactive regulatory state in a disease model suggests that common mechanisms are operative in orderly gonadal withdrawal under hostile or inappropriate environments and may underly the reversibility of human uremic hypogonadism with successful renal transplantation.

Timing of sexual receptivity and the release of gonadotrophins during puberty in female rats

In about 60% of rats that were paired with fertile males before vaginal opening, vaginal opening occurred between 15:00 and 21:00 h under controlled lighting conditions (lights on 06:00-18:00 h). No rats mated before 12:00 h or after 03:00 h. Most of the rats (52/82) mated within 3 h after vaginal opening. About 90% of the rats that were paired with fertile males before vaginal opening mated and most conceived. Serum LH and FSH levels rose from 14:00 h to a peak at 18:00 h, whereas hypothalamic LHRH content suddenly decreased by 18:00 h. This study shows that the timing of sexual receptivity, ovulation and the release of gonadotrophins during puberty are similar to those at pro-oestrus in adult rats and suggest that the diurnal rhythm of hormonal changes plays an important role in timing of the first oestrus.

Puberty-related increase in episodic LHRH release from rat hypothalamus in vitro.

The retrochiasmatic hypothalamus (RCH) was removed from brains of male rats between 12 and 50 days of age, and immediately studied in vitro. The release of LHRH from the RCH was evaluated by periodic (7.5-min) collections of culture medium and subsequent RIA. With synthetic LHRH in the experimental system, the mean (+/- 1 SD) recovery was 94 +/- 7% with a variation coefficient of 14 +/- 3%. An increase in LHRH release was considered to be significant when it exceeded 6 pg/7.5 min. Biological viability of RCH in vitro was assessed by an increased release of LHRH in response to the depolarizing effect of veratridine. As age increased, from 12 to 50 days, the hypothalamic LHRH content steadily increased. However, a significant increase in veratridine - induced release of LHRH occurred only at 23 days and thereafter. At various ages, single hypothalami were studied during a mean 112-min period to evaluate the spontaneous release of LHRH. In all age groups, the in vitro LHRH release occurred in pulses. However, mean pulse frequency increased significantly with age: in 12- and 17-day-old rats, 0.3 pulse/112 min was observed; at 23, 25 and 27 days, this frequency varied between 1.8 and 3.0 pulses/112 min. At 50 days of age, the observed frequency was within the same range. We conclude that the RCH obtained from rats of various ages may retain in vitro its capacity to release LHRH episodically and that the frequency of these episodic pulses markedly increases with age to the time of the onset of puberty in male rats.