摘要:

To determine whether norepinephrine (NE) will stimulate gonadotropin secretion in androgenized female rats, we administered NE (0.3 µM in 2 µl saline; pH 6.0–6.5) into the third ventricle of females which had been treated neonatally with two different doses of testosterone propionate (TP; 10 or 100 µg) on day 5 of life. This treatment rendered these animals anovulatory as evidenced by polyfollicular ovaries and a persistent vaginal estrus condition which occurred by 100 days of age. Those females which were determined to be anovulatory were ovariectomized 4 weeks prior to the stereotaxic implantation of an intracerebroventricular (ICV) cannula. Ten to twelve days following cannula placement, animals were primed with either estradiol benzoate (EB; 30 µg) or EB and progesterone (P; 5 mg). Two days following steroid priming, NE was infused into the third ventricle at 15.00 h and blood samples were taken via an intra-atrial catheter at 15-min intervals for 2 h before and 2 h after administration. In both TP-treated groups, NE caused rapid and significant (p < 0.01) elevations in plasma luteinizing hormone (LH) concentrations when animals were primed with EB as compared with control females given acid saline infusions (pH 6.0–6.5). Similar responses to NE were seen after additional priming with P at the same time as EB. Follicle-stimulating hormone (FSH) values did not increase following NE or saline infusion to any of the groups. These data suggest that the ability of the female to respond to NE with increases in plasma LH is present following androgenization, and the possibility exists that NE may be a component of the neural trigger for phasic LH secretion which is lost following neonatal exposure to a

ISSN:0028-3835    

DOI:10.1159/000124539

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Brain histamine levels were determined in golden hamster hypothalamus and ‘brain minus hypothalamus’ on each of the 4 days of the estrous cycle and on selected days of pregnancy. The highest histamine content of the hypothalamus was observed on day 3 of the estrous cycle. The highest histamine content of the hypothalamus was observed on day 3 of the estrous cycle, which is the day prior to recurrence of heat on day 4. Day 4 terminates in ovulation. The histamine level in the remainder of the brain peaked on day 2. During gestation the histamine content of the ‘brain minus hypothalamus’ was greatest on day 5, while the maximum content of histamine in the hypothalamus was not reached until day 8. After the 8th day of pregnancy, there was an overall decline in brain histamine that continued until parturition. The hypothalamic histamine level in nonpregnant females was not different from that of males. However, in the remainder of the brain, histamine levels in females on days 1 and 2 of the estrous cycle were higher than i

ISSN:0028-3835    

DOI:10.1159/000124540

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Acute stress promotes the secretion of prolactin (PRL) and of proopiomelanocortin (POMC)-derived peptides, adrenocorticotropic hormone and β-endorphin, from the pituitary into the systemic circulation. The present study evaluates the influence of recurrent stress upon the biosynthetic activity of cells secreting these hormones in the rat. Chronic, intermittent, electrical foot-shock (3 mA 1 s duration, every 5 s for 30 min, twice daily) over a period of 1, 3 or 7 days caused an increase in messenger ribonucleic acid (mRNA) levels coding for POMC in the anterior pituitary. Maximally elevated mRNA levels were achieved after 3 days treatment (about 80% in excess of control values) which showed no further change at 7 days. These elevated levels of POMC mRNA were associated with increased levels of immunoreactive (ir)-β-endorphin in the adenohypophysis following 7 days of stress treatment. In contrast, this treatment did not significantly alter mRNA levels coding for PRL in the anterior pituitary. Similarly, POMC mRNA levels in the intermediate/posterior pituitary were also not significantly altered during exposure to repeated stress. Similar changes in the biosynthesis of the pituitary hormones were seen in rats suffering from chronic arthritic pain for 3 weeks: there was an approximately 80% increase in POMC mRNA levels in the anterior pituitary which was associated with an increase in the levels of ir-β-endorphin in this lobe and an increase in the plasma levels of ir-β-endorphin. In contrast, there were no changes in the levels of mRNA coding for PRL in the adenohypophysis. Moreover, levels of POMC mRNA and of ir-β-endorphin in the intermediate/posterior pituitary remained unchanged. It is concluded that although lactotrophic and corticotrophic cells of the adenohypophysis and corticotrophic cells in the intermediate pituitary respond similarly to acute stress stimuli with an increased secretion, the biosynthetic activity of these cells is differentially modulated under chronic st

ISSN:0028-3835    

DOI:10.1159/000124541

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Arachidonate and its metabolites may play an important role in the release of prolactin. In the present study, the effect of maitotoxin, a calcium channel activator, was measured on the release of arachidonate and its metabolites from the prolactin-secreting 7315a tumor. Maitotoxin increased the release of prolactin, arachidonate, prostaglandins E2 and F2α (PGE2, PGF2α) and leukotriene C4 (LTC4) from 7315a cells prelabeled with [3H]arachidonate. The magnitude of the increase of prolactin and arachidonate release was decreased in low-calcium medium. The release of arachidonate from cellular phospholipids is necessary for the effect of maitotoxin on prolactin release because quinacrine, an inhibitor of arachidonate hydrolysis from phospholipids, blocked the maitotoxin-induced release of prolactin. The ability of maitotoxin to induce prolactin release appears to require metabolic transformation of arachidonate to its metabolites because BW755c, an inhibitor of the conversion of arachidonate, blocked the maitotoxin-induced prolactin release. In particular, LTC4 may be an important component of the prolactin release process because nordihydroguaiaretic acid and nafazatrom, which block the production of leukotrienes and other lipoxygenase-generated products, decreased LTC4 and prolactin release without affecting arachidonate, PGE2 or PGF2α production. In contrast, indomethacin, a prostaglandin synthesis inhibitor, decreased PGE2 and PGF2α production without affecting LTC4 or prolactin release. These data indicate that release of LTC4 and prolactin are closely linked events in 7315a tumor ce

ISSN:0028-3835    

DOI:10.1159/000124542

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

The present study was designed to characterize the time and dose relationships of the response of tuberoinfundibular dopaminergic (TIDA) neurons in the rat to systemically administered prolactin (PRL). The activity of TIDA neurons was estimated by measuring the rate of dopamine (DA) synthesis in the median eminence (DOPA accumulation following the administration of a decarboxylase inhibitor). Rats were pretreated with bromocriptine, a dopaminergic agonist, so as to inhibit the release of endogenous PRL from the anterior pituitary, and thereby reduce the activity of TIDA neurons to a ‘basal’ level from which it could be increased subsequently by exogenously administered PRL. In control animals an intraperitoneal injection of ovine PRL (oPRL) increased DOPA accumulation at 16 h, but not before, whereas in bromocriptine-pretreated animals an intraperitoneal injection of oPRL increased DOPA accumulation after 4 h (‘tonic’ component) and caused a further increase after 16 h (‘induction’ component). Continuous intravenous infusions of oPRL into bromocriptine-pretreated rats increased DOPA accumulation in the median eminence by 4 h, and when infused into control rats oPRL reduced serum concentrations of endogenous rat PRL (rPRL) by 2 and 4 h. Continuous intravenous infusions of rPRLincreased DOPA accumulation in the median eminence after 2 h; this effect exhibited a very steep dose-response relationship (possibly an ‘all-or-none’ response). TIDA neurons were very sensitive to changes in circulating concentrations of PRL; their activity was increased if serum PRL concentrations were merely doubled by infusing a low concentration of rPRL for 4 h. Three daily injections of haloperidol elevated circulating rPRL concentrations and increased the rate of DOPA accumulation in the median eminence. These effects were blocked by an injection of bromocriptine 4 h prior to sacrifice. In animals with ‘induced’ TIDA neurons (i.e., treated for 3 days with haloperidol and 4 h with bromocriptine), a 2-hour intravenous infusion of rPRL increased the rate of DOPA accumulation in the median eminence; the time of onset and dose of rPRL needed to trigger this effect in ‘induced’ TIDA neurons were not different from those in ‘control’ neurons. On the other hand, the magnitude of the increase in DOPA accumulation in response to intravenous infusions of rPRL was markedly increased in the ‘induced’ TIDA neurons. Thus, TIDA neurons that have been ‘induced’ by chronically elevated circulating concentrations of PRL exhibit a greater response to the acute administration of PRL. These results suggest that the magnitude of the activation of TIDA neurons by acute changes in circulating PRL concentrations (‘tonic’ component) is determined by the preceding history of circulating concen

ISSN:0028-3835    

DOI:10.1159/000124543

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Previous studies in our laboratory [Endocrinology 114:1605–1612 (1984); Neuroendocrinology 41:252–257 (1985)] examined the influence of ovarian steroids on pulsatile luteinizing hormone (LH) release, and involved immediate replacement following ovariectomy (OVX) of estradiol (E2) and progesterone (P) for a 24-hour period within the physiological context of the estrous cycle. The present study investigated the effects of replacing E2 and/or P 1 week after OVX, and therefore examined whether the time elapsed following OVX influences the effects of ovarian steroids on pulsatile LH release. Immediately after jugular venous cannulation, rats were implanted with either empty silastic capsules or capsules capable of restoring physiological levels of E2 and/or P comparable to those found in intact rats between the intervals of diestrus 1 (Dl) and diestrus 2 (D2), or D2 and proestrous morning. 24 h later, these rats were bled continuously at a rate of 50 µl whole blood/6 min for 3 h for analysis of pulsatile LH secretion. Rats with empty capsules had decreased levels of E2 and P and elevated mean blood LH levels, pulse amplitudes and frequencies. Two groups of animals with E2 capsules had plasma E2 levels comparable to those seen either in the D1-D2 or D2-proestrous intervals, decreased levels of P, and in both cases significant decreases in LH pulse amplitude, but no change in LH pulse frequency or basal LH secretion. Since mean blood LH levels in 8-day ovariectomized rats are determined by LH pulse amplitude, frequency and basal LH secretion [Neuroendocrinology 37:421–426 (1983)], the E2-induced effects on LH pulse amplitude were not sufficient to decrease mean blood LH levels. Rats with P capsules had physiological D1-D2 plasma levels of P and decreased levels of E2, but no change in any parameter of pulsatile LH release. Rats implanted with both E2 and P capsules had physiological D1-D2 levels of both steroids which caused a significant decrease in mean blood LH levels, due to decreases in LH pulse amplitude and pulse frequency. There was no significant difference in the extent of the decrease in pulse amplitude produced by E2 (low) or E2 (low) + P. This indicates that the decreased LH pulse amplitude following E2 (low) + P is due to the E2 (low) alone. The suppressive effects on LH pulse amplitude produced by E2 (low or high) were mediated centrally, since the in vitro responses to LHRH of anterior pituitary (AP) fragments from E2-implanted rats were greater than those of AP fragments from rats implanted with empty capsules. When compared with our previous studies, the present results demonstrate that some of the responses of the pulsatile LH secretory system to the negative feedback effects of ovarian steroids remain the same, while others are altered when these same levels of steroids are replaced for 24 h 1 week after OVX rather than immediately after OVX. D2-proestrous levels of E2 retain their suppressive action on LH pulse amplitude, D1-D2 levels of E2 + P combined remain effective in decreasing pulse frequency and D1-D2 levels of E2 are again ineffective in altering pulse frequency. In contrast, D2-proestrous E2 levels lose their suppressive action on LH pulse frequency, D1-D2 levels of P lose their action in decreasing pulse amplitude and D1-D2 levels of E2 gain the ability to suppress LH pulse amp

ISSN:0028-3835    

DOI:10.1159/000124544

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

One hundred and forty human fetal pituitary glands were removed from fetuses at 7–40 weeks of gestation and studied by light microscopy and immunocytochemistry to localize adenohypophysial hormones. For immunocytology, the avidin-biotin-peroxidase complex technique was more sensitive and identified hormones in younger fetuses than did the immunoperoxidase method. Adrenocorticotrophin, β-endorphin, and growth hormone were the first hormones detected; they were identified by intense cytoplasmic immunopositivity at 8 weeks of gestation. Between 10 and 20 weeks, many growth hormone containing cells were large and showed scattered, faint positivity; after 20 weeks, smaller cells with intense positivity predominated. α-Subunit of the glycoprotein hormones was identified at 9 weeks of development; β-sub-units of thyroid-stimulating hormone, follicle-stimulating hormone, and luteinizing hormone appeared by 12 weeks. Gonadotrophs differed in numbers related to fetal age and sex. From 15 to 25 weeks, glands of female fetuses contained more gonadotrophs than did those of males; after 25 weeks, there was no significant difference in total gonadotroph numbers. Throughout gestation, adenohypophyses of male fetuses had more luteinizing hormone containing cells than follicle-stimulating hormone containing cells; pituitaries of females had approximately the same numbers of follicle-stimulating hormone containing and luteinizing hormone containing cells. Prolactin was identified in few small cells at 12 weeks; at term, prolactin-containing cells were numerous, comparable to those seen in the hyperplasia of maternal glands in late gestation and during lactation. This comprehensive study indicates morphologic correlations with pituitary hormone extraction data and with the appearance of the various hormones in the fetal circula

ISSN:0028-3835    

DOI:10.1159/000124545

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

In the Djungarian hamster, short photoperiods induce regression of testes and accessory glands. There is evidence that the length of time melatonin levels are elevated is the signal conveying the photoperiodic effects to the neuroendocrine axis. When the temporal course of decompression of the pattern of pineal melatonin content was followed after a change from long to short photoperiods by symmetrical extension of the dark time, extension proceeded first into the morning hours. The present study investigated whether, after transition from long to short photoperiods by either extending the dark period into the morning hours, or starting the darktime at noon, differences in the gonadal reaction and in the rate of extension of the pineal pattern ensue. Three and 7 weeks after transition from long to short photoperiods highly significant differences were found in the rate of involution of testes and accessory glands. Regression was more advanced after extension of the dark period into the morning hours. The length of time that pineal melatonin content was elevated also differed markedly between the two groups. After 3 weeks in short photoperiods, the length of the melatonin peak was more than 9 h when the dark period was extended into the morning, but only about 7 h if it was extended into the afternoon. It is suggested that the different rate of gonadal regression after different ways of transition into the same photoperiod is due to the different rate of decompression of the melatonin pattern.

ISSN:0028-3835    

DOI:10.1159/000124562

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

This study was performed to determine if two sex differences in gonadotropin responses to negative feedback, the acute postcastration rise and the effect of follicular fluid (FF) in the acute castrate, could be reversed by neonatal treatment with sex-opposite steroids. Female rats that received testosterone propionate (TP-females) and male rats that received estradiol benzoate (EB-males) neonatally were studied as adults. EB-males showed an LH response to gonadecto-my which was much less than control males, and did not differ from control females, which could suggest the hypothesis that neonatal estrogen ‘feminizes’ the male response to gonadectomy. However, as the postgonadectomy response in both LH and FSH was depressed in both TP-females and EB-males in comparison to their respective matched sex controls, neonatal steroid treatment appears simply to impair hypothalamic-pituitary function. This is not a result of decreased pituitary responsiveness to GnRH in TP-females and EB-males. On the other hand, neonatal steroid treatment does not change the sex-specific response to imposition of peptide negative feedback (i.e., FF administration). In control and TP-females, FF significantly suppressed serum FSH levels, both in intact animals and 9 h after gonadectomy. In both control and EB-males, FF suppressed FSH in intact animals, but failed to do so in acute castrates. Thus, neonatal steroid treatment does not reverse the sex differences in gonadal-gonadotropin interrelations, but rather causes an impairment in the acute recognition of loss of negative feedback at the hypothalamic le

ISSN:0028-3835    

DOI:10.1159/000124546

出版商:S. Karger AG    

年代:1986

数据来源: Karger

摘要:

Picrotoxin (1 mg/kg, i.p.) and a high dose of diazepam (10 mg/kg, i.p.) increased the concentration of plasma corticosterone in nonstressed rats. This effect of diazepam was unaffected by picrotoxin and bicuculline (GABA-A receptor blockers), atropine (a muscarinic receptor blocker), apomorphine (a dopamine receptor agonist), haloperidol (a dopamine receptor blocker) and yohimbine (an alpha-2-adrenergic receptor blocker); but was blocked by clonidine (an alpha-2-receptor agonist) and this effect of clonidine was reversed by yohimbine. Diazepam was unable to elevate plasma corticosterone levels in rats pretreated with dexamethasone. Clonidine and the GABA-B receptor agonist, baclofen, failed to affect the picrotoxin-induced rise of plasma corticosterone, but this rise was abolished by a low dose of diazepam (1 mg/kg). The results suggest that the diazepam-induced enhancement of ACTH release, presumably mediated by blockade of alpha-2-adrenergic receptors, is responsible for the observed increase of plasma corticosterone level in rats. On the other hand, the elevation of plasma corticosterone induced by picrotoxin appears to be mediated by GABA-A receptors.

ISSN:0028-3835    

DOI:10.1159/000124547

出版商:S. Karger AG    

年代:1986

数据来源: Karger