Biomedical subjects

W G Rossmanith

Publications and source records attributed to W G Rossmanith.

At least 37 records · Page 2Linked to original sources

PubMed1996

Inhibition of steroid-induced galanin mRNA expression in GnRH neurons by specific NMDA-receptor blockade.

Galanin mRNA levels in GnRH neurons increase in association with a steroid-induced LH surge in female rats. Both the steroid-induced LH surge and the concomitant increase of galanin mRNA in GnRH neurons are blocked by non-specific inhibition of central nervous system activity imposed by pentobarbital and specific central alpha-adrenergic receptor blockade. Based on these observations, we hypothesized that galanin gene expression in GnRH neurons is induced whenever GnRH neurons become activated to generate an LH surge. If this were the case, then any neurotransmitter receptor blocking agent that inhibits the LH surge by central mechanisms would likewise block the associated increase in galanin mRNA in GnRH neurons. We tested this hypothesis by examining the effects of an N-methyl-D-aspartate (NMDA) receptor antagonist on the steroid-induced LH surge and on levels of galanin mRNA in GnRH neurons. Three groups of ovariectomized rats were used: Group 1 -treated with estradiol and progesterone (E/P) and sacrificed at the peak of the LH surge; Group 2-treated the same as Group 1 except that dizocilpine (MK801, an NMDA receptor antagonist) was used to block the LH surge; and Group 3-treated the same as Group 1 except they received vehicle instead of E/P. Double-and single-label in situ hybridization followed by computerized image analysis were used to measure levels of galanin mRNA and GnRH mRNA in GnRH neurons [as grains/cell (g/c)]. E/P treatment induced a 3-fold increase in LH levels and a 5-fold increase in the galanin mRNA signal content of GnRH neurons. Treatment with MK801 completely prevented the LH surge in all animals and also blocked the steroid-induced increase in galanin mRNA in GnRH neurons. As assessed by 2 independent GnRH single-labeled assays, neither GnRH message content nor the number of identifiable GnRH neurons differed among the experimental groups. We conclude that the increase in galanin mRNA levels in GnRH neurons is tightly coupled to the occurrence of a steroid-evoked LH surge, and we infer that induction of galanin gene expression in GnRH neurons is induced as a consequence of synaptic activation of GnRH neurons.

Animals↗

PubMed1996

Induction of galanin mRNA in GnRH neurons by estradiol and its facilitation by progesterone.

On the day of proestrus in the rat, rising plasma levels of estradiol (E) act in concert with progesterone (P) to trigger a preovulatory release of gonadotropins. Cellular levels of galanin mRNA in GnRH neurons are increased in association with the proestrous surge of gonadotropin secretion; however, the relative contribution made by E and P to the induction of galanin mRNA expression in GnRH neurons is unknown. We investigated the role of E and P in the induction of galanin gene expression in GnRH neurons by examining the effects of different combinations of E (estradiol benzoate; 50 micrograms and P (5 mg)) on the LH surge and the concomitant induction of galanin mRNA in GnRH neurons. We sacrificed ovariectomized adult rats after 1 of 4 treatments: Group 1: vehicle control (n = 6); Group 2: P alone (n = 7) Group 3: E alone (n = 7); Group 4: combined E/P (n = 6); the animals were killed at 18.00 h at the time of the LH surge. The brains from these animals were processed by double-label in situ hybridization to allow measurement of galanin mRNA levels in GnRH neurons. GnRH neurons were identified with a digoxigenin-labeled cRNA probe for GnRH mRNA, and galanin mRNA was detected and measured simultaneously with an 35S-labeled cRNA probe coupled with computerized grain counting. Estimation of cellular levels of GnRH mRNA was accomplished with single-label in situ hybridization, an 35S-labeled GnRH cRNA probe and computerized grain counting. We observed a 3-fold induction of galanin mRNA in the GnRH neurons of animals treated with E alone compared with those treated with the vehicle alone (vehicle: 13 +/- 2 vs E: 42 +/- 4 grains/cell (g/c); P < 0.01); LH levels in the E-treated animals were elevated, albeit moderately, with respect to the vehicle controls. Compared with vehicle-treated animals, those treated with the combination of E and P showed a 5-fold induction of galanin mRNA in GnRH neurons (68 +/- 9 g/c), which was significantly (P < 0.01) greater than that observed in the animals treated with E alone; in addition, the magnitude of the LH surge was much greater (P < 0.05) in the E/P-treated group compared with the E alone group. In contrast, compared to the vehicle controls, animals treated with P alone (15 +/- 2 g/c) showed no discernable effect on galanin mRNA levels; moreover, no LH surge occurred in the P alone group. Neither the number of identified GnRH cells nor their content of GnRH mRNA differed significantly among the experimental groups (GnRH mRNA signal: vehicle controls: 153 +/- 6 vs E: 159 +/- 6 vs E/P: 153 +/- vs P: 148 +/- 8 g/c). We conclude that while E is the primary ovarian signal inducing galanin mRNA expression in GnRH neurons and the LH surge itself, P plays a facilitatory role in both of these processes.

Animals↗

PubMed1996

Galanin gene expression in hypothalamic GnRH-containing neurons of the rat: a model for autocrine regulation.

Increasing experimental evidence has accumulated to suggest that galanin may be one of the essential regulators in the reproductive system of the rat. Galanin is a polypeptide which has been found in hypothalamic neurons, where it is colocalized with GnRH. GnRH-containing cells begin to express detectable levels of galanin mRNA at the onset of puberty, and this process is dependent on the presence of the gonads. This indicates that the induction of galanin expression in GnRH neurons is an important requirement for the maturation of the reproductive axis. The pattern of co-expression of galanin and GnRH in hypothalamic neurons is sexually dimorphic, with much greater galanin mRNA content in the GnRH neurons of females compared to males. The role of galanin may therefore be important in reproductive processes unique to the female, such as the LH surge and ovulation. During the estrous cycle, galanin mRNA levels are enhanced in GnRH neurons at the time of the LH surge. This suggests a tight coupling of galanin biosynthesis and release to the activity state of the GnRH neurons. Expression of the galanin gene in GnRH neurons is regulated by ovarian sex steroids: estradiol appears to support the basal expression of galanin mRNA in GnRH neurons. In addition, estradiol is capable of dramatically increasing galanin gene expression, either when administered alone or in conjunction with progesterone. Nevertheless, neuronal activation with concomitant induction of galanin gene expression requires transsynaptic signals by afferent inputs impinging on the GnRH cells. Galanin may serve as a critical autocrine regulator for the activity of GnRH cells, in that it may be co-released with GnRH and act presynaptically on the GnRH neuron, helping to shape GnRH release into distinct pulses. Collectively, these observations indicate that galanin gene expression in GnRH neurons may represent a pivotal signal for the activation of the neuroendocrine reproductive axis.

Animals↗

PubMed1995

[Clinical and endocrine effects of laparoscopic ovarian surgery in patients with polycystic ovary syndrome].

OBJECTIVES: Is minimal invasive ovarian surgery an alternative infertility treatment for patients with polycystic ovary (PCO) syndrome? METHODOLOGY: 52 anovulatory patients with the clinical and endocrine characteristics of PCO syndrome were treated with laparoscopic Nd: YAK (n = 11) or CO2 (n = 41) laser surgery to drain atretic follicles and destroy the ovarian stroma. RESULTS: Following surgical reduction of serum androgen and estrogen levels (p < 0,01), 83% of the PCO patients ovulated spontaneously or following ovulation induction; pregnancies occurred in 38%. At re-laparoscopies, 86% of patients had no periovarian adhesions. CONCLUSIONS: Since laparoscopic laser surgery is capable of inducing profound clinical and endocrine effects, it may represents a feasible alternative for infertility treatment in PCO patients.

Adult↗

PubMed1995

Stimulated thyrotropin and prolactin secretion in lactating and non-lactating women.

During the postpartum period, lactation is initiated by a massive release of prolactin which, in turn, reflects reduced dopaminergic inhibition of the pituitary lactotrophs. This postpartum prolactin rise can be prevented by administration of dopamine agonists. The release of thyrotropin (TSH) is also controlled by dopaminergic inputs and, therefore, TSH secretion may also be affected by postpartum alterations in dopaminergic activity. To gain further insight into the regulation of TSH and prolactin secretion during the postpartum period, we compared the basal and stimulated TSH and prolactin levels of postpartum lactating (n = 10) and non-lactating women (treated with 5 mg bromocriptine daily, n = 9) with those of normal cycling women (n = 9). Frequent blood samples were obtained on postpartum day 5 or in the early follicular phase before and after administration of thyrotropin-releasing hormone (TRH) for serial determination of TSH and prolactin by immunoradiometric assay (IRMA). Based serum prolactin levels were high (p < 0.001) in lactating women and low in both non-lactating and normal cycling women. When these differences in the basal prolactin concentrations were taken into account, the stimulated prolactin release (relative prolactin increase and area under the prolactin curve) was found to be highest (p < 0.05) in non-lactating women and lowest in lactating women. Basal TSH secretion was not significantly different between the groups of women (p > 0.2). Yet, both the relative TSH increases and the response curves following TRH stimulations were high (p < 0.05) in normal cycling women and low in both lactating and non-lactating postpartum women. These observations confirm a difference in the basal and stimulated prolactin release between lactating and non-lactating women. They also indicate that the TRH-stimulated TSH release is greatly affected by the postpartum state, irrespective of lactation or therapeutic weaning. The observation of a decreased sensitivity of pituitary thyrotrophs in concert with unchanged basal TSH secretion is suggestive of changes in hypothalamic TRH secretion and/or in the TSH metabolic half-life during the postpartum period.

Adult↗

PubMed1994

Management of peritoneal hemorrhage due to follicle rupture under anticoagulation therapy.

Severe bleeding into the peritoneal cavity from a ruptured ovulatory follicle is a rare complication in women receiving anticoagulation therapy. A number of both surgical and non surgical methods have been proposed to solve this problem. We adopted a novel therapeutic approach in a 40-year old patient who presented with recurrent acute hemoperitoneum under anticoagulation therapy for combined cardiac valve disease. The hemoperitoneum was successfully managed twice by laparoscopy. The patient then received intranasal GnRH analogue treatment together with transdermal estradiol and oral medroxyprogesterone-acetate. In this way ovarian sex steroids were replaced while cessation of ovarian function was achieved by the hypogonadotrophic condition. At the end of this mode of treatment no recurrence of a hemoperitoneum was seen in our patient. We therefore suggest that considerable gains may be expected from this method for the management of recurrent acute peritoneal hemorrhage caused by ovulation bleeding in patients under anticoagulation therapy.

Adult↗

PubMed1994

Serotoninergic control of gonadotrophin and prolactin secretion in women.

OBJECTIVE: Due to conflicting observations from previous investigations, the role of serotonin (5-HT) in the regulation of the human menstrual cycle has not been clearly established. We have therefore investigated the possible participation of 5-HR in the control of gonadotrophin and PRL secretion in women, using the potent 5-HT3 receptor antagonist ondansetron as a pharmacological probe. DESIGN: Serum profiles of LH, FSH and PRL were obtained in 9 normally cycling women during a control and a treatment cycle, during which ondansetron (8 mg orally) was administered daily. On day 10 of both cycles, the serum pulsatility of LH, FSH and PRL was assessed by frequent blood sampling (at 10-minute intervals for 10 hours). Pituitary responsiveness was tested by administration of a GnRH bolus (25 micrograms i.v. after 8 hours). MEASUREMENTS: LH, FSH and PRL were serially determined in all blood samples by immunofluorescence assays. The resulting hormone data arrays were searched for significant fluctuations by the Cluster pulse algorithm. RESULTS: Compared with control cycles, the temporal organization and the endocrine characteristics of the treatment cycles remained virtually unaltered. Serotonin antagonism did not noticeably affect the LH pulse attributes (frequencies, interpulse intervals, amplitudes). Although FSH amplitudes declined markedly (P < 0.05), the remaining pulse attributes were unchanged. A clear increase (P < 0.05) in the PRL pulse frequency was noted, while PRL pulse amplitudes tended to increase (P = 0.1). Gonadotrophin and PRL release in response to GnRH administration was unaltered by ondansetron treatment. CONCLUSIONS: Serotoninergic blockade by a selective 5-HT3 receptor antagonist failed to modify pulsatile LH secretion, but induced distinct changes in episodic FSH and PRL secretion. Since the pituitary gonadotrophin and PRL responsiveness remained unaltered during 5-HT3 receptor blockade, the observed alterations in the FSH and PRL secretion presumably relate to altered hypothalamic regulation of these pituitary hormones. Thus, the central regulation of pulsatile FSH and PRL release in women appears to involve 5-HT3 receptor-mediated processes.

Adult↗

PubMed1994

Neuroendocrinology of aging in humans: attenuated sensitivity to sex steroid feedback in elderly postmenopausal women.

Studies in experimental animals have shown that the sensitivity of the hypothalamic-pituitary system to ovarian sex steroid feedback declines while aging progresses. Since similar observations are lacking in humans, we studied the gonadotropin secretion of postmenopausal women (PMW) of different ages before and following a 7-day course of oral clomiphene citrate (CC, 100 mg daily). For serial determinations of serum luteinizing hormone (LH) and follicle-stimulating hormone (FSH) levels, blood was sampled frequently from 5 younger PMW (mean age 55.2 years) and 6 older PMW (mean age 80.3 years) for 10 h. Eight hours after initiation of blood sampling, gonadotropin-releasing hormone (GnRH, 25 micrograms) was administered. Compared to untreated conditions, CC administration did not significantly change the serum concentrations of the estrogens (estrone, estradiol) and androgens (testosterone; androstenedione, dehydroepiandrosterone sulfate). However, CC increased the sex hormone-binding globulin levels in both younger and older PMW, suggestive of the estrogenic effects of this compound. In the unstimulated secretory profiles of younger PMW, mean LH levels decreased (p < 0.05) in response to CC, presumably a consequence of decreased (p < 0.05) pulse frequencies, but not pulse amplitudes. Likewise, by virtue of decreased (p < 0.05) FSH pulse amplitudes, FSH levels declined (p < 0.05) in younger PMW. In contrast, both the LH and FSH levels and their pulsatility remained virtually unaltered following CC administrations to older PMW. The GnRH-mediated gonadotropin release was uneffected by CC administrations in either group of PMW.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗

PubMed1994

Activation-dependent regulation of galanin gene expression in gonadotropin-releasing hormone neurons in the female rat.

In rats, galanin is colocalized in GnRH neurons, and galanin mRNA in GnRH neurons is increased coincidentally with the preovulatory gonadotropin surge. Whether the induction of galanin mRNA in GnRH neurons at proestrus reflects the action of sex steroids is unknown. We tested this hypothesis by challenging ovariectomized rats (n = 7) with estrogen and progesterone (E/P) to induce a LH surge and measuring galanin mRNA in GnRH neurons to determine whether there was an associated induction of galanin message in these cells. We used single and double label in situ hybridization and image analysis to compare among groups the levels of both galanin mRNA and GnRH mRNA in GnRH neurons. We found that steroid-primed animals showed an approximately 400% induction of galanin mRNA signal in GnRH neurons over that in vehicle-treated animals. Second, we hypothesized that steroid-dependent events which induce the expression of galanin mRNA in GnRH neurons depend on transsynaptic input to GnRH neurons. We tested this hypothesis by examining the effect of a pharmacological blockade of the steroid-induced activation of GnRH neurons on levels of galanin mRNA in these cells. We killed groups of ovariectomized adult female rats at the peak of a E/P-primed LH surge (n = 7) and after steroid priming followed by blockade of the LH surge with either the general anesthetic pentobarbital (n = 7) or the specific alpha-adrenergic receptor blocker phenoxybenzamine (n = 7). When we examined signal levels representing galanin mRNA content in GnRH neurons, we observed a 4-fold increase in signal for galanin mRNA in the GnRH neurons of steroid-primed (E/P surge) animals compared with that in oil-treated controls (P < 0.0004). This increase in galanin mRNA was prevented when the LH surge was blocked by treatment with either pentobarbital or phenoxybenzamine (P < 0.03 and P < 0.0001 vs. E/P surge controls, respectively). Cellular levels of GnRH mRNA were not different among control, E/P, and E/P plus pentobarbital groups (P > 0.2). These observations suggest that an increase in galanin mRNA levels in GnRH neurons is tightly coupled to the occurrence of a LH surge. By inference, induction of galanin mRNA in GnRH neurons reflects their activation, possibly via afferent neurons that transduce the steroid signal to GnRH neurons.

Animals↗

PubMed1994

Induction of galanin gene expression in gonadotropin-releasing hormone neurons with puberty in the rat.

The onset of puberty reflects the developmental activation of GnRH neurons whose secretory activity awakens the reproductive axis; however, the cellular mechanisms involved in this activational process remain poorly understood. GnRH neurons coexpress the neuropeptide galanin, and we have previously shown that galanin's level of coexpression is linked to the activity state of GnRH neurons. We theorized that altered expression of galanin by GnRH neurons may be an important mechanism related to activation of GnRH neurons at puberty. We examined two hypotheses related to this idea. First, we tested the hypothesis that expression of galanin messenger RNA (mRNA) in GnRH neurons is induced across the transition from prepubertal to adult life in the rat. To accomplish this, we used double label in situ hybridization and image analysis to compare cellular levels of galanin mRNA in GnRH neurons between groups of prepubertal and adult male and female rats. Levels of galanin mRNA within GnRH neurons increased significantly across puberty in both sexes. In females, galanin mRNA signal in GnRH neurons increased approximately 8-fold, whereas in males, cellular galanin mRNA signal levels increased about 2-fold. The number of identifiable GnRH neurons was not significantly different among the experimental groups. Next, we examined the hypothesis that pubertal induction of galanin mRNA in GnRH neurons reflects the activational effects of gonadal hormones associated with the onset of puberty. To test this, we killed groups of prepubertal male and female rats together with adult male and female animals that had been either castrated or sham castrated at a prepubertal age. In animals that had been prepubertally castrated, no developmental increase in galanin mRNA in GnRH neurons was observed, whereas in sham-castrated animals, levels of galanin mRNA in GnRH neurons were again shown to be higher in adult compared to prepubertal animals of both sexes, as had been demonstrated in the first experiment. We conclude that galanin message expression in GnRH neurons is induced during the transition from the juvenile to the adult state through a gonad-dependent process. This developmental increase in galanin gene expression is one mechanism by which the capacity for the synthesis and secretion of galanin by GnRH neurons may be enhanced, which, in turn, could facilitate the functional activity of GnRH neurons and amplify their trophic effect on the pituitary.

Animals↗

PubMed1994

Does the gonadotropin pulsatility of postmenopausal women represent the unrestrained hypothalamic-pituitary activity?

Ovarian sex steroids profoundly modulate the gonadotropin pulsatile secretion in women. A gonadotropin pulsatility determined in the absence of any considerable ovarian sex steroid feedback, as in postmenopausal women (PMW), may thus represent the unrestrained activity of the hypothalamic-pituitary axis. We hypothesized that increases in the gonadotropin pulse frequencies and amplitudes during sex steroid replacements may be limited by those determined in the hypogonadal state of PMW. To address this assumption, we investigated the unstimulated the gonadotropin-releasing hormone (GnRH)-stimulated release of luteinizing hormone (LH) and follicle-stimulating hormone (FSH) in PMW before and during sequential ovarian sex steroid treatments. Seven PMW (mean age 59.4 years) were studied initially during unreplaced conditions (control studies), then on the last day of a 21-day course of oral estradiol valeriate (E2) administrations (2 mg daily) and, finally, on the last day of a 21-day course of oral estradiol-progesterone (E2/P4) replacements (2 mg of E2 and 200 mg of micronized P4 daily). On all study occasions, blood was drawn at 10-min intervals for 10 h and GnRH (25 micrograms iv) was administered 8 h after initiation of blood collections. Compared to control conditions, the basal serum estrogen (estrone and E2) and progesterone (P4) concentrations markedly increased (p < 0.001) following oral E2 or E2/P4 treatments. As determined by Cluster pulse algorithm, LH and FSH were found to be released episodically during each study condition. Mean LH and FSH release rates declined (P < 0.05 or less) during E2 and E2/P4 regimens.(ABSTRACT TRUNCATED AT 250 WORDS)

Androgens↗

PubMed1994

The distribution of hypothalamic nitric oxide synthase mRNA in relation to gonadotrophin-releasing hormone neurons.

Using probes for rat neural nitric oxide synthase (NOS) mRNA and GnRH mRNA, we performed in situ hybridization to survey NOS mRNA distribution within the hypothalamus of the male and female rat and sought evidence for its expression in GnRH neurons. The NOS cRNA probe was radiolabelled with 35S, and a digoxigenin-labeled rat GnRH cRNA probe was used for double-label studies. NOS mRNA was localized in discrete hypothalamic areas, in grain clusters suggestive of individual neurons. NOS mRNA-positive cells were located mainly in the supraoptic and paraventricular nucleus, particularly overlying the magnocellular division. Rostrally, cells expressing NOS mRNA were especially prominent in the diagonal band of Broca, in a distribution very similar to GnRH neurons. Nevertheless, only one of 370 cells labeled for GnRH mRNA appeared to be positive for NOS mRNA. We conclude that NOS mRNA is located prominently in regions where CRH, AVP and oxytocin cells are located. NOS mRNA-positive cells are located in close proximity to GnRH neurons, but rarely do such neurons express NOS mRNA.

Amino Acid Oxidoreductases↗

PubMed1994

Autonomous gonadotropin release from the human pituitary in vitro and factors influencing this secretion.

Our understanding of the hypothalamus as the sole pacemaker for episodic hormone release has been challenged by recent observations of an autonomous rhythmic secretion from the pituitary, independent of hypothalamic inputs. Using an in vitro perifusion system, we were able to demonstrate an intrinsically pulsatile gonadotropin secretion from human fetal and adult pituitaries. This high-frequency/low-amplitude release is calcium-dependent and stimulated by gonadotropin releasing hormone (GnRH) administrations. Also, the autonomous release of luteinizing hormone (LH) appears to be temporally and functionally linked to the spontaneously pulsatile secretion of other anterior pituitary hormones, suggesting the existence of a common intrapituitary mechanism entraining these hormone pulsatilities. Further, the spontaneous and GnRH-stimulated LH release is greater from human female fetal pituitaries than from male fetal pituitaries at mid-gestation, presumably a reflection of differences in the negative feedback actions by factors from the fetal gonads. Collectively, we have observed an autonomous gonadotropin release from the human pituitary independent of, but facilitated by, GnRH. This spontaneous pulsatile secretion is calcium-dependent and entrained to the release of other anterior pituitary hormones. Therefore, it may represent the activity of a common intrapituitary pulse-generating mechanism and its modulation by factors from inside and outside the human pituitary.

Calcium↗

PubMed1994

Role of androgens in the regulation of the human menstrual cycle.

Although previous investigations have examined the importance of androgens in the regulation of the human menstrual cycle, no consensus has been reached, due to conflicting results. We have therefore used the non-steroidal anti-androgen flutamide as a pharmacological probe to evaluate the role of androgens in the control of gonadotropin secretion in normally cycling women. Eight women were studied during control and treatment cycles, during which either placebo (as control) or flutamide (750 mg orally) was given daily. Blood was sampled every other day during the follicular and luteal phases and daily around the expected midcycles for determination of luteinizing hormone (LH), follicle stimulating hormone (FSH), estradiol, progesterone and androgens (testosterone, androstenedione, dehydroepiandrosterone sulfate) by radioimmunoassay and immunoradiometric assay. To establish unstimulated and gonadotropin releasing hormone (GnRH)-stimulated gonadotropin profiles, blood samples were frequently collected (every 10 min for 8 h, GnRH 25 micrograms i.v. after 7 h on day 10 in both the control and treatment cycles. Compared to control conditions, the durations of both the follicular and luteal phases did not change considerably during flutamide treatments. Serum androgen levels (testosterone, androstenedione, dehydroepiandrosterone sulfate) were significantly (p < 0.01) reduced during androgen antagonism. Daily gonadotropin and estradiol levels did not differ between control and flutamide cycles, while progesterone secretion tended to be attenuated (p = 0.2) during the luteal phases of the flutamide cycles. The LH and FSH secretory profiles and the GnRH-stimulated gonadotropin responses remained virtually unchanged during androgen antagonism.(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1993

Contemporary insights into the control of the corpus luteum function.

Increasing evidence has been accumulated to confirm the critical dependency of the corpus luteum function from regular pituitary luteinizing hormone (LH) inputs. In fact, close temporal and functional links have been demonstrated between intermittent LH stimulations and episodic sex steroid release emanating from the mature corpus luteum. Moreover, an intrinsically pulsatile progesterone (P4) release independent of, but facilitated by gonadotropin inputs has been observed from the corpus luteum in vitro. This may suggest some functional autonomy in this organ, at least within close temporal limits. The pulsatile P4 secretion may be optimally maintained by gonadotropin stimulations effected at frequencies and amplitudes similar to those observed during the luteal phase in vivo. Since autonomous P4 secretion is modulated, amongst other determinants, by prostaglandins, oxytocin and P4 itself, ultra-short feedback loops are assumed to exist for an optimal tuning of the luteal function. This episodic sex steroid release from the corpus luteum may be required to set the endocrine signal for the blastocyst to implant.

Animals↗

PubMed1993

[Effects of sleep on gonadotropin secretion].

Comparable to the period of adolescence in puberty, sleep exerts profound effects on the gonadotropin secretion in adult women. During the early follicular phase of the menstrual cycle, a slowing of the luteinising hormone (LH) pulse frequencies is concomitant with a rise in LH pulse amplitudes during sleep. A selective sleep-associated increase in opioidergic, but not in dopaminergic activity, may account for the decline in the LH pulse frequencies. Since pituitary gonadotropin responsiveness is virtually unchanged during sleep, the reasons for the enhanced LH pulse amplitudes remain unknown. Although the physiological meaning of this neuroendocrine manifestation is unexplained at present, the observed changes in the LH secretory profiles during sleep may represent close functional links between the endocrine secretion and the rest-activity cycle of the brain.

Adolescent↗

PubMed1993

Ultradian and circadian patterns in luteinizing hormone secretion during reproductive life in women.

Based on the findings of close links between intermittent hypothalamic releasing hormone stimulation and hypophyseal gonadotrophin response, an assessment of the pulsatility of serum gonadotrophins may represent a feasible way to indirectly evaluate central regulatory processes in humans. Since ovarian steroid feedback is virtually absent in hypogonadal women, their luteinizing hormone (LH) pulsatility may represent the unrestrained LH pulse rhythm at its maximal rate. Relative changes in the LH pulse characteristics during the menstrual cycle could then be referred to this basic pulsatility. Hence, LH pulse frequencies increase during cycle periods of high sex steroid exposure, but this increase is limited to the LH periodicities found in hypogonadal women. Furthermore, LH pulse amplitudes are successively enhanced from the follicular to the luteal phase of the cycle yet they never exceed those found in hypogonadal subjects. In addition, circadian excursions subserve pulsatile LH secretion during all periods of the menstrual cycle, although the character of these circadian rhythmicities differs from that observed in the LH secretory profiles of hypogonadal women. Thus, albeit profoundly modulated by ovarian sex steroid feedback during the menstrual cycle, LH pulsatility and its circadian variations in women during the menstrual cycle is confined to the ultradian and circadian LH secretory patterns of the hypogonadal state.

Activity Cycles↗

PubMed1993

Chronobiology of prolactin secretion in women: diurnal and sleep-related variations in the pituitary lactotroph sensitivity.

While a nocturnal rise accounts for the marked circadian variability of prolactin (PRL) secretion in humans, the mechanisms subserving this neuroendocrine manifestation are still obscure. Since gonadotropin-releasing hormone (GnRH) stimulates PRL under physiological conditions, we questioned whether changes in the pituitary lactotroph sensitivity to GnRH during the 24-hour cycle may contribute to the expression of circadian PRL rhythmicity. Accordingly, 8 women were studied in the early follicular phase of their cycles (days 2-5) on 6 occasions in random order: during daytime between 10.00 and 14.00 h ('day' studies), at night between 22.00 and 02.00 h, when the women were awake ('night' studies), and finally, during the identical night hours, when the women were asleep ('sleep' studies). On all occasions, blood was collected at 10-min intervals for 4 h, while either GnRH (25 micrograms i.v. bolus) or saline (as control) was injected twice within 2 h. As assessed by the net PRL increments (differences between unstimulated nadir and stimulated peak) and the areas under the PRL response curves, the PRL secretion was not substantially altered following GnRH stimulations during the day studies. In contrast, PRL release was markedly enhanced (p < 0.05 or less vs. day studies), when GnRH was administered during the night studies. This GnRH-stimulated PRL release was even further increased (p < 0.01 vs. day, p < 0.05 vs. night or saline studies), when GnRH had been given during sleep.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗