Prostaglandin E2-induced luteinizing hormone-releasing hormone release involves mobilization of intracellular Ca+2.

The present in vitro experiments were performed to examine the involvement of Ca+2 in the mechanism by which prostaglandin E2 (PGE2) induces LHRH release from the median eminence (ME) of the hypothalamus. Stepwise decreases in the Ca+2 concentration of the incubation medium reduced the LHRH response to PGE2. Nevertheless, neither complete omission of Ca+2 (residual Ca+2 concentration, 3.

Physiological peripubertal activation of the ovary is not reproduced by pregnant mare serum gonadotropin (PMSG) administration.

During the days preceding the first ovulation the ovary of the rat exhibits a remarkable increase in estradiol (E2) and progesterone (P) release in response to gonadotropins. No such increase is observed in the case of androgens (A, testosterone + dihydrotestosterone). The present experiments were undertaken to examine the possibility of reproducing these developmental events by stimulating the ovary with a gonadotropin that has substantial FSH-like activity.

Release of prostaglandin E2 from the hypothalamus depends on extracellular Ca2+ availability: relation to LHRH release.

The present experiments were performed to investigate the role of extracellular Ca2+ in the process of prostaglandin E2 (PGE2) release from the median eminence (ME) of the hypothalamus. Changes in the release of LHRH were also evaluated. Incubation of ME fragments with different concentrations of K+ induced a dose-related increase in PGE2 and LHRH release.

Maternal modulation of infantile ovarian development and available ovarian luteinizing hormone-releasing hormone (LHRH) receptors via milk LHRH.

In the rat, ovarian LHRH receptor content, measured by the binding of [125I]D-Ala6-Pro9-LHRH ([125I]A-LHRH) to ovarian membranes, declines during the days preceding the first preovulatory LH surge. The present results show that LHRH receptor content is low during neonatal-infantile days (days 5-15) and increases markedly thereafter to a maximum by day 25. When ovarian membranes from 10-day-old rats were pretreated with MgCl2 to dissociate endogenously bound hormone, LHRH-binding capacity increased to levels similar to those in untreated ovaries from 25-day-old rats.

Effect of selective removal of the adrenal medulla on female sexual development.

The ovary and adenohypophysis of the rat contain beta-adrenergic receptors and respond to beta-adrenergic stimulation with hormone release. To determine the importance of the adrenal medulla as a source of adrenergic influences regulating prepubertal ovarian and pituitary function, a technique was developed to remove most of the adrenal medulla without compromising adrenocortical function. Medullectomy (MED) of 24-day-old female rats depressed both spontaneous diurnal changes in plasma epinephrine (EPI), and the EPI and norepinephrine (NE) response to decapitation, without affecting corticosterone (B) levels.

Effect of experimental alterations in serum levels of 5 alpha-androstane-3 beta,17 beta-diol on the timing of puberty in the female rat.

It has been suggested that in the rat, 5 alpha-androstane-3 alpha,17 beta-diol (3 alpha-diol) is physiologically involved in restraining the onset of female puberty. To test this hypothesis several experiments were performed. In normal rats, serum levels of 3 alpha-diol decline slightly during the initial phases of puberty and then sharply several hours before the afternoon preovulatory LH surge on the day of first proestrus.

An automated system for the study of pulsatile hormone secretion in the immature rat.

A procedure is described for prolonged sampling of blood from unrestrained immature rats which overcomes some of the problems associated with contemporary techniques. 1 or 2 days before sampling, the animal is fitted with two indwelling catheters, one inserted into the right jugular vein and the other into a femoral vein. On the day of the experiment blood is continuously withdrawn from the jugular vein (30 microliter/min) using a peristaltic pump and is dispensed into sample tubes every 5 min by means of an automatic fraction collector.

Ovarian adrenergic nerves play a role in maintaining preovulatory steroid secretion.

Little is known about the role of ovarian nerves in the control of steroid secretion. We have examined the effect of sectioning the adrenergic superior ovarian nerve (SON) on the secretion of progesterone (P), and estradiol (E2) from the ovary. The steroids were measured in blood samples collected every 4 min from the ovarian vein in the proestrous and estrous phases of the rat estrous cycle.

Prepubertal ovarian function is finely regulated by direct adrenergic influences. Role of noradrenergic innervation.

In the rat, the main source of adrenergic fibers innervating nonvascular ovarian tissue is the superior ovarian nerve (SON). To determine the influence of the SON on prepubertal ovarian function and, hence, on the time of puberty, several experiments were conducted. Transection of the SON in early juvenile rats (day 24) led to more than 60% depletion in ovarian norepinephrine (NE) content, but affected neither the timing of vaginal opening nor that of first ovulation.

Neuroendocrine mechanisms controlling the onset of female puberty: the rat as a model.

The advent of female puberty represents the culmination of a diversity of developmental processes which affect all components of the reproductive axis. Development of neuroendocrine reproductive functions proceeds in a harmonious and interrelated manner. No unique 'trigger' of puberty can be discerned, but rather puberty represents the climax of a cascade of events, finely interconnected throughout the continuum of sexual maturation.

Hyperprolactinemia enhances ovarian estrogen responsiveness to gonadotropins in prepubertal rats: antagonistic effect of adrenalectomy.

Hyperprolactinemia (HP) induced in female rats by dopaminergic receptor blockers enhanced ovarian estradiol (E2) release in response to human chorionic gonadotropin (hCG) or human follicle-stimulating hormone (hFSH) in vitro. Uterine weight and ovarian aromatase activity were also increased. In contrast, ovarian androgen (A) release in response to hCG was reduced.

Novel hypothalamic arachidonate products stimulate somatostatin release from the median eminence.

Arachidonic acid (AA) stimulates the in vitro release of somatostatin (SRIF) from the hypothalamic median eminence (ME). This effect is inhibited by 5, 8, 11, 14-eicosatetraynoic acid (ETYA) but not by indomethacin (ID). Microsomal fractions from the rat hypothalamus catalyze an NADPH-dependent metabolism of AA to form several oxygenated products of which the major metabolites are 5, 6-epoxyeicosatrienoic acid (5, 6-EET) and its hydration product, 5, 6-dihydroxyeicosatrienoic acid (5, 6-DHET).

Peripubertal decline in ovarian LHRH receptor content: characterization and distribution.

In the rat, ovarian LHRH receptor content, as measured by the binding of 125I-D-Ala6, Pro9-LHRH (A-LHRH) to ovarian membranes, decreases markedly during the days preceding the first preovulatory gonadotropin surge. The present study shows that the decrease in LHRH receptor number occurs exclusively in granulosa cells, and that the greatest rate of decline takes place between the juvenile period and the early proestrous phase of puberty. In contrast to granulosa cells, membranes prepared from ovarian tissues after removal of these cells demonstrated no significant change in LHRH binding capacity throughout puberty.

Pulsatile luteinizing hormone (LH) patterns in ovariectomized rats: involvement of norepinephrine and dopamine in the release of LH-releasing hormone and LH.

Cannulated ovariectomized (OVX) rats were bled every 10 min for 2 h to characterize their individual patterns of LH release. After the last sample, all rats were decapitated, and their brains were removed for analysis of LHRH, norepinephrine (NE), and dopamine (DA) levels in median eminence (ME), arcuate-ventromedial, and suprachiasmatic-medial preoptic region (Sch-PO) to determine if changes in NE, DA, and LHRH levels in any of those areas could be observed at different points during the pulsatile release of LH. The results showed that when LH levels started to increase, NE levels peaked in the Sch-PO, whereas a sharp drop in DA and LHRH levels in the ME was detected, which may reflect an acute release in the ME of both DA and LHRH.

Changes in aromatase activity in the rat brain during embryonic, neonatal, and infantile development.

We assessed the activity of the aromatase enzyme complex in slices of brain from rats by measuring the release of 3H2O from [1 beta-3H]testosterone. In hypothalami from 12-day-old rats, the rate of aromatase activity was linear with time and amount of tissue. The reaction was saturated at a substrate concentration of 0.

Pituitary LHRH receptors during puberty in the female rat: is the proestrous decline in receptor content due to occupancy?

As during the adult estrous cycle, the number of pituitary luteinizing hormone-releasing hormone (LHRH) receptors was found to increase prior to the first preovulatory surge of LH. Receptor content, as measured by the binding of the analog 125I-D-Ala6-Pro9-LHRH to pituitary membranes, declined markedly at the time of the first LH surge, remaining low during the first estrus and first diestrus. When pituitary membranes from animals undergoing an LH surge were incubated with MgCl2 to dissociate endogenously bound hormone, available binding sites were restored to pre-LH surge values.

Studies on the central effect of prolactin in inducing precocious puberty in the female rat.

Implantation of prolactin (PRL) into the median eminence (PRL-ME implants) of 23 day old female rats markedly advanced the onset of puberty, as measured by the age at vaginal opening and at first ovulation. Precocious puberty was preceded by steroidogenic activation of the ovary, as reflected by increases in uterine weight and an enhanced in vitro steroidal responsiveness of the ovary to hCG. The stimulatory effect of PRL-ME implants could not be attributed to alterations in the release of LH, FSH, GH or TSH from the anterior pituitary.

Evidence for involvement of alpha-adrenergic receptors in norepinephrine-induced prostaglandin E2 and luteinizing hormone-releasing hormone release from the median eminence.

Studies were conducted to determine if the stimulatory effect that norepinephrine (NE) exerts on the release of prostaglandin E2 (PGE2) and LHRH from the median eminence is mediated by alpha- or beta-adrenergic receptors. Incubation of median eminence fragments from adult male rats with different concentrations of phentolamine, an alpha-receptor antagonist, resulted in a dose-related inhibition of the release of both PGE2 and LHRH induced by NE, with an IC50 of 3.5 X 10(-7) and 0.