摘要:

This study was designed to examine possible relationships between the photoperiodic regulation of prolactin secretion and the activity of dopaminergic and GABAergic neurons projecting to the external layer of the median eminence. The study was carried out on the mink whose remarkable photosensitivity has been clearly demonstrated. The animals were reared in short (4L:20D) or long (20L:4D) photoperiods. The experiment began in November when day length is short (9.5 h). Dopaminergic and GABAergic neurons were studied using immunocytochemical methods allowing evaluation of the immunoreactivities of tyrosine hydroxylase (TH) and glutamate decarboxylase (GAD), which are respective markers of these neurons. The results were quantified by image analysis. The plasma prolactin level of animals maintained in 4L:20D decreased after 60 days and TH and GAD immunoreactivity were strongly stimulated. After 110 days, the prolactin concentration and TH and GAD immunoreactivity recovered their starting levels. In animals maintained in 20L:4D, the prolactin level was 3 times higher than at the beginning of the photoperiodic treatment but only dopaminergic neurons showed a change, i.e. a decrease in immunoreactivity. At the end of the experiment, prolactin secretion was no longer affected by the stimulatory effect of long-day treatment, and TH immunoreactivity remained low. These results confirm the generally accepted concept that dopaminergic neurons are potent PIF-producing components. GABAergic hypothalamic system appears to be implicated in photoperiodic PRL regulation, but this remains to be clearly demonstrated.

ISSN:0028-3835    

DOI:10.1159/000125771

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The effects of ventromedial hypothalamic (VMH) lesions on the circadian periodicity of blood corticosterone were studied in female rats. The rats were kept on a 12-hour light/12-hour dark illumination regimen and fed ad libitum. Three, 10 and 12 weeks after the VMH lesions, the concentrations of blood corticosterone were measured every 4 h for 48 h in the same unanesthetized rats. Three weeks after the operation, the circadian rhythm in VMH-lesioned rats was disturbed and disappeared. The corticosterone levels at 03:00, 07:00, and 11:00 were significantly higher than those in sham-operated rats. 10 and 12 weeks after the operation, the circadian rhythm, however, was notable (p < 0.05, p < 0.05). The elevated mean corticosterone levels over 48 h at 3 weeks after the operation decreased at 10 and 12 weeks. The sham-operated rats showed a significant circadian rhythm at 3, 10 and 12 weeks after the operation (p < 0.001 in each period) with a peak concentration at 19:00 and through at 07:00. These findings show that the corticosterone circadian rhythms which were disturbed in the dynamic phase after VMH lesions recovered in the static phase of obesity, suggesting that the ventromedial hypothalamus is not an essential biological clock of circadian corticosterone rhythm.

ISSN:0028-3835    

DOI:10.1159/000125772

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The secretion of gonadotropins and the role exerted by the endogenous opioid system on luteinizing hormone (LH) secretion were investigated in 6 postmenopausal women affected by idiopathic Parkinson’s disease (PD) as well as in 6 age- and weight-matched normal postmenopausal women as controls. The mean plasma follicle-stimulating hormone (FSH) and LH levels were evaluated both under basal conditions and after 20 days of conjugated estrogen administration (1.25 mg/day). At the same time, the activity of the endogenous opioid system was evaluated, as well as the LH response to the 4-hour infusion of the opioid antagonist naloxone (1.6 mg i.v. bolus followed by 1.6 mg/h). Both before and during estrogen administration, plasma FSH levels were similar in the two groups of subjects, whereas plasma LH levels were significantly lower (p < 0.01) in parkinsonian than in control women. In each subject estrogen administration significantly blunted (p < 0.01) plasma FSH levels. Plasma LH levels were reduced only in controls (p < 0.05), but not in women with PD. In each subject, before estrogen administration, the plasma LH levels did not vary during naloxone infusion. In control women after 20 days of estrogen administration, the plasma LH levels significantly increased during naloxone infusion (p < 0.01). By contrast, in women with PD, conjugated estrogens failed to restore the LH response to naloxone. The present results suggest that the neurotransmitter mechanisms, which regulate LH secretion, are altered, and, in particular, the activity of the endogenous opioid system is deficient in women with P

ISSN:0028-3835    

DOI:10.1159/000125773

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The effect of chronic (35 days) and selective sodium or chloride depletion on the regulation of angiotensin II receptors in the anterior pituitary gland of young male rats was studied by quantitative autoradiography. Both chronic sodium or chloride depletion produced significant extracellular fluid volume contraction, stimulation of the circulating renin-angiotensin system and increased the number of angiotensin II receptors in the anterior pituitary gland. Changes in angiotensin II receptors in both sodium- and chloride-depleted animals were associated with increased plasma prolactin levels. Our results suggest a participation of the pituitary renin-angiotensin system in the physiological response and/or possible adaptation to chronic sodium or chloride depletion. Extracellular fluid volume contraction and profound chronic stimulation of the circulating renin-angiotensin system may contribute to regulate anterior pituitary angiotensin II receptors and may influence prolactin release.

ISSN:0028-3835    

DOI:10.1159/000125774

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Pituitaries from 24 human fetuses at 7–20 weeks of gestation were studied in culture to assess hormone release, response to adenohypophysiotropic hormones and cytodifferentiation by electron microscopy in cultures lasting 4–8 days and in some cases up to 28 days. At 7 weeks of gestation, ACTH was released by cultured cells which included recognizable corticotrophs. GH was released by cells cultured from 8- to 9-week fetuses and densely granulated somatotrophs were present in the cultures. α-Subunit of glycoprotein hormones was present in cultures from 10-week fetuses and TSH and LH were released from 12-week fetuses. FSH was found in cultures of a 13-week female fetus but not before 14 weeks in cultures from males. The levels of FSH and LH were higher in media from cultures of females than from those of males at all ages from detection to 20 weeks, whereas α-subunit was slightly higher in media from males. While cells with features of the glycoprotein hormone cell line were found in cultures from 10-week fetuses, no characteristic thyrotrophs or gonadotrophs were recognized. PRL was not measured in basal incubations before 14 weeks. The amounts of all hormones released were proportional to fetal age and decreased with duration of culture. Cortisol suppressed ACTH release in cultures from 7- to 8-week fetuses. Responsiveness of GH release to GRH/SRIH, of ACTH to CRH, and of FSH to GnRH, was found at 12 weeks; LH stimulation by GnRH and TSH response to TRH were documented at 14 weeks. Increments of gonadotropin release during incubation with GnRH were greater in cultures from females than in those from males. PRL release responded to GRH stimulation and to SRIH inhibition in parallel with GH; this behavior is consistent with production of both hormones by mammosomatotrophs. The onset of hormone release by cultured human fetal pituitaries correlates with the detection of hormones biochemically and immunohistochemically. Responsiveness of fetal adenohypophysial cells to hormonal influences indicates functional maturity early in gest

ISSN:0028-3835    

DOI:10.1159/000125775

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

To study the role of corticotropin-releasing hormone (CRH) in the circadian rhythm of circulating corticotropin (ACTH), β-endorphin (β-END), corticosterone, and prolactin (PRL), we measured the effects of CRH immunoneutralization over a 24-hour period in chronically cannulated, conscious, freely moving, male Sprague-Dawley rats, maintained at a constant light-dark cycle. Blood samples were collected in the morning (08.00 h), at noon (12.00 h), and in the evening (18.00 h) on the day of treatment, and in the morning (08.00 h) of the next day. Hyperimmune rabbit serum raised against rat CRH (1.0 ml/rat, i.v.) or normal rabbit serum (NRS, 1.0 ml/rat, i.v.) was administered at 08.00 h, immediately after the first blood sample had been collected. CRH immunoneutralization caused no significant decreases in circulating immunoreactive ACTH, β-END and corticosterone plasma levels at noon, but abolished the evening rises of these hormones. PRL levels were not significantly different between the groups at any time point measured. To compare the effects of CRH immunoneutralization to those of glucocorticoid negative feedback, we measured the effects of dexamethasone (0.5 mg/kg, i.v. at 08.00 h) on the above parameters. ACTH and β-END concentrations were significantly decreased, and corticosterone and PRL levels were markedly suppressed after glucocorticoid administration both at 12.00 and 18.00 h. However, 24 h after the administration of dexamethasone, PRL concentrations were elevated despite persistently low corticosterone levels. These data suggest that evening elevations of ACTH, β-END, and corticosterone depend on release of endogenous CRH, while CRH does not appear to play a significant role in maintaining baseline ACTH and β-END levels in the morning, and resting PRL levels throughout th

ISSN:0028-3835    

DOI:10.1159/000125776

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

In vivo and in vitro methods have been used to compare the effects of opioid receptor blockade on the functional activity of the hypothalamo-pituitary-gonadal axis in adult (200 g) and sexually immature (50 g) male rats. In the adult, a single injection of the µ-receptor antagonist, naloxone (500 µg/100 g body weight, s.c), produced hypersecretions of luteinizing hormone (LH) and testosterone. Maximal serum concentrations of the two hormones were attained within 20 and 60 min respectively. In contrast, neither ICI 174864 (100 µg/100 g body weight, s.c.) nor MR2266 (150 µg/100 g body weight, s.c), which block δ- and ĸ-receptors respectively, stimulated pituitary-gonadal activity; indeed, like the saline vehicle, both tended to depress the serum LH concentration. The injection procedure was sufficient to activate the hypothalamo-pituitary-adrenal axis and, thus, the vehicle-treated controls exhibited significant increases in the plasma adrenocorticotrophin and serum corticosterone concentrations. These effects were enhanced by naloxone (500 µg/100 g body weight, s.c.) and by the ĸ-opioid receptor (MR2266, 150 µg/100 g body weight, s.c.) but not by the δ-opioid receptor antagonist (ICI 174864, 30–100 µg/100 g body weight, s.c). The increases in serum corticosterone and LH concentration induced by naloxone in adult rats were not apparent in the sexually immature (50 g) animals. To the contrary, in the young rats naloxone (250 and 500 µg/100 µg body weight, s.c.) attenuated, in a dose-dependent manner, the pronounced hypersecretion of corticosterone induced by the vehicle injection. The higher dose of the antagonist (500 µg/100 g body weight, s.c.) also overcame the significant reductions in serum LH evident 20 (p < 0.05) and 40 (p < 0.01) min after the saline injection but the lower dose (250 µg/100 g body weight, s.c.) was ineffective in this respect. In vitro, hypothalami from both adult and sexually immature rats responded to the addition of naloxone (10–8–10–6M) to the incubation medium with significant (p < 0.01) concentration-dependent increases in the release of gonadotrophin-releasing hormone (GnRH). In contrast, ICI 174864 (10"7–10–6M) and MR2266 (10-7–10-6M) had little effect on the secretion of the releasing hormone by hypothalami from rats of either group although, at the highest concentration tested, MR2266 (10–6M) precipitated a small increase in GnRH release from hypothalami from adult rats. The secretory responses of hypothalami from adult and prepubertal rats to naloxone were inhibited by the inclusion in the medium of the αi-adrenoceptor antagonist alfuzosin (10-6M) which, in the absence of naloxone, had no discernible effects on GnRH release. Receptor binding studies indicated that both the density and affinity of naloxone-sensitive opioid binding sites within the hypothalamus were similar in adult and sexually immature rats. The results demonstrate marked differences between the neuroendocrine responses of adult and sexually immature rats to opioid receptor blockade which, with respect to the secretion of GnRH, cannot be explained by immaturity of the receptors or

ISSN:0028-3835    

DOI:10.1159/000125777

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

The effects of various stressors (restraint, ether, histamine and insulin-induced hypoglycemia stress) on the early time course activation of the different catecholaminergic (CA) cell groups A1/C1, A2/C2 and locus ceruleus (LC) from the brainstem were studied. The activity of the central noradrenergic neurons was assessed by measuring in tissue punches the 3,4-dihydroxyphenylacetic acid (DOPAC) level, a side metabolite of noradrenaline (NA) and adrenaline biosynthesis that is thought to reflect the activity of NA cells. Short 5 min restraint stress led to an immediate increase of DOPAC level in the three CA groups. In the A1/C1 and A2/C2 groups the maximal increase, respectively + 75 and + 50%, was already reached at the end of the application of the stress while for the LC the maximum (+84%) was obtained 15 min after the onset of the stress. Return to baseline level was achieved within 2 h. Continuous immobilization stress did not further alter the DOPAC concentration in the LC and the Al/Cl while a progressive increase up to 85% in the A2/C2 group was seen over 20 min. Following a 2-min exposure to ether, DOPAC was increased in all three structures within 5 min. At this time the maximum was already reached in the A1/C1 and LC, respectively +99 and +43%. After histamine or insulin injection DOPAC level increased in the A1/C1 and A2/C2 in the +25/+50% range but was not significantly affected in the LC. In all the stress situations studied the increase in DOPAC level, particularly in the Al/Cl group always preceded or was concomitant to the increase of plasma corticosterone. While our results confirm the well-known increase of the activity of the CA neurons following stress, they reveal clear-cut differences in the time course of the early activation as well as in the sensitivity of the various brainstem CA groups for different stressors. The rapid response and maximum amplitude which could be seen within 5 min is compatible with the hypothesis that the CA cells could be involved in the stimulation of the hypothalamic-pituitary-adrenal axis elicited by the stressors.

ISSN:0028-3835    

DOI:10.1159/000125778

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

To test the hypothesis that one aspect of growth hormone (GH) regulation involves a direct effect of GH on its own secretion at the level of the pituitary, we evaluated the effects of human GH on basal and GH-releasing factor (GRF > induced GH secretion in rat and bovine pituitary cell cultures. Both 4 h (acute) and 24 h (chronic) exposure of bovine pituitary cells to exogenous human GH significantly (p < 0.001) reduced GH secretion. Acute treatment resulted in a decrease in GH secretion from 579 ± 24 to 500 ± 17 ng/ml 4 h(mean ± SEM, n = 24) while chronic treatment resulted in a GH decrease from 595 ± 21 to 483 ± 17 ng/ml/4 h. In contrast, human GH treatment of rat somatotropes had no effect on basal GH secretion. GRF-stimulated GH secretion was not affected by either acute or chronic GH exposure in either species. These results demonstrate that there are species-specific differences in the ability of GH to regulate its own secretion and provide evidence for a direct inhibitory effect of GH at the level of the bovine pitui

ISSN:0028-3835    

DOI:10.1159/000125779

出版商:S. Karger AG    

年代:1991

数据来源: Karger

摘要:

Dopamine (DA) from both the posterior pituitary (PP) and stalk-median eminence (SME) inhibits prolactin (PRL) secretion from the anterior pituitary. Estradiol participates in the regulation of PRL release, in part by modulating DA release from the SME. However, little is known concerning the effects of estradiol on the release of DA from the PP. The objective of this study was to examine whether estradiol rapidly affects the potassium-evoked release of endogenous DA from the PP and SME in vitro. Tissues were dissected from ovariectomized rats and allowed to equilibrate in media for 30 min.Two pulses of 28 mM K+, 3 min each, were then given 30 min apart. Test substances were added 20 min before the second stimulus. DA in the media was determined by HPLC. Estradiol, at a concentration of 1 and 10 nM, significantly stimulated the potassium-evoked DA release from the PP by 34 and 47%, respectively. This stimulation was specific since 17α-estradiol, a biologically inactive isomer, and testosterone, were without effects. Estradiol did not alter DA release from either the SME or isolated neural lobes of the PP. Naloxone, an opioid receptor antagonist, abolished the estradiol-induced stimulation of DA release from the PP. In contrast, amphetamine, a DA-releasing agent, significantly increased DA release in the presence of naloxone. In conclusion, estradiol stimulates DA release from the PP but not the SME or neural lobe; this effect is rapid and stereospecific, and the effects of estradiol appear to be mediated via an opioid(s) peptide(s) from the intermediate lobe

ISSN:0028-3835    

DOI:10.1159/000125780

出版商:S. Karger AG    

年代:1991

数据来源: Karger