摘要:

Luteinizing hormone releasing hormone (LHRH) administered to ovariectomized marmosets treated with a low dose of 17β-oestradiol significantly enhanced proceptivity within 2 h. Without oestradiol priming LHRH treatment did not produce this effect. The dose of LHRH given did not significantly alter plasma levels of cortisol or progesterone. The behavioural effect of this treatment is therefore likely to have been mediated via a direct central action rather than indirectly through stimulating adrenocortical steroid secretion. These results provide the first demonstration that LHRH can potentiate the proceptive behaviour of a female primate

ISSN:0028-3835    

DOI:10.1159/000124218

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

We have previously shown that chelated copper stimulates the release of luteinizing hormone releasing hormone (LHRH) from explants of the median eminence area (MEA) incubated under in vitro conditions and that this stimulation involves a ligand-specific interaction. In this study, we addressed the question: do testicular steroids regulate the secretory response of LHRH neurons to copper? MEA, obtained from immature, mature, immature castrated and sham-operated rats, were incubated in the presence of various concentrations of copper for 15 min and then in the absence of copper for an additional period of 30 min. We noted that after a lag period of 5 min of incubation, the rate of LHRH release increased in a linear fashion for a period of 15 min. In addition, the rate of LHRHrelease as well as the rate at which LHRH release was accelerated were saturable functions of the concentration of copper. When incubation was carried out in the presence of a nonsaturating concentration of copper (50 µM), the fractional amount (percent of the total MEA content) of LHRHreleased from the MEA of castrated rats was significantly (p < 0.001) lower than that from sham-operated rats; stimulated release being 0.9% and 1.4%, respectively. Similarly, copper-stimulated release from the MEA of immature rats was lower than that from the MEA of mature rats. However, when incubation was carried out in the presence of saturating concentrations of copper (100 or 200 µM), the precentage of stimulated release from the MEA of castrated rats was similar to that of sham-operated rats and it was about 2.8%. In addition, we found that LHRHcontent of the MEA of immature and castrated rats was significantly lower than that of mature and sham-operated rats, respectively. To estimate the size of the releasable pool of LHRHin the MEA of these animals, we maximally stimulated LHRH release with 60 mM K+. It was found that, regardless of the physiological state of the animals, about 2.6% of the MEA content was released. These results suggest that: (1) copper interacts with a limited number of sites on the LHRH neuron; (2) testicular steroids regulate the process of copper-stimulated release of LHRH by increasing the affinity of these interactive sites to copper; (3) testicular steroids increase the size of the releasable pool of LHRH in the median eminence, and (4) the size of the releasable pool is proportional to the MEA content of the peptide and this proportionality is not steroid-dependent. We propose that testicular steroids regulate two important aspects of the secretory function of the LHRH neuron: the capacity of the neuron to release LHRH and the affinity of the copper-interactive sites for coppe

ISSN:0028-3835    

DOI:10.1159/000124219

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Male rats were exposed to the smoke from 2 cigarettes every morning for a total period of 9 days. The next day they were decapitated immediately after the exposure to the smoke from 4 cigarettes (Kentucky reference IR-1 type) burned at 30-min intervals. Control animals were exposed to air alone or to nicotine-free cigarette smoke (Cambridge glass fibre filters). In contrast to chronic exposure to filtered smoke, exposure to unfiltered smoke resulted in a 10% increase in catecholamine (CA) levels (quantitative histofluorimetry) within the lateral palisade zone, the posterior periventricular hypothalamic nucleus and within the dorsomedial hypothalamic nucleus. There was also an increase in amine turnover (tyrosine hydroxylase inhibition by α-methyl-dl-p-tyrosine methylester; αMT) in the dopamine (DA) systems of the medial and lateral palisade zones and in the periventricular noradrenaline (NA) hypothalamic systems. Chronic exposure to unfiltered cigarette smoke resulted in reductions of prolactin, LH and FSH levels (radioimmunoassay). Following αMT treatment chronic exposure to unfiltered cigarette smoke still led to reduced prolactin serum levels. In addition an increased vasopressin serum concentration was found. The effects of chronic exposure to cigarette smoke on neuroendo-crine function and on hypothalamic CA systems are suggested to be mediated via nicotine. Combined with the results from a previous study the present results indicate that tolerance does not develop with regard to the inhibitory effects of exposure to cigarette smoke on prolactin, LH and FSH secretions. The same is true for the stimulatory effects on the tubero-infundibular DA neurons and the periventricular NA systems. But chronic exposure to cigarette smoke seemed to induce tolerance with regard to its stimulatory effects on subependymal, dorsomedial and paraventricular hypothalamic NA systems and on corticosterone relea

ISSN:0028-3835    

DOI:10.1159/000124220

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Cysteamine (β-mercaptoethylamine, MEA) is a naturally occurring sulfhydryl compound that depletes pituitary PRL, causes a reduction in brain and gut somatostatin (SRIF), and suppresses norepinephrine (NE) and epinephrine (EPI) synthesis by inhibition of dopamine-β-hydroxylase (DBH). SRIF inhibits GH and TSH secretion, whereas, NE and EPI facilitate their release. The objectives of this investigation were to: (1) determine the dose-response and time course of DBH inhibition by MEA in vivo and in vitro, and correlate these findings with MEA tissue levels, and (2) assess the function of SRIF and NE/EPI in regulation of episodic GH and TSH secretion using MEA. Animals were administered MEA (75–300 mg/kg, s.c.) and hypothalamic levels of dopamine (DA), NE, EPI, serotonin (5-HT) and MEA were measured by high-performance liquid chromatography (HPLC) and electrochemical detection. DBH activity was measured in vitro after exposure to MEA ± N-ethylmaleimide (NEMI). Chronically cannulated rats were administered MEA (100 or 300 mg/kg) and serial blood samples were removed in undisturbed animals, and after 30 min swimming stress. Cannulated rats with bilateral lesions of the ventromedial/arcuate nuclei (VMN/ARC) were administered MEA (150 mg/kg). MEA caused a dose-related decrease in NE/EPI and in increase in DA at doses >150 mg/kg. Tissue MEA was highest at 4 h (679 ± 64 pM/mg tissue), but still measureable after 24 h. MEA inhibited DBH in vitro (95% inhibition at 10–3M); NEMI blocked inhibition. Stress-induced GH supression and corticosterone release were partially blocked by a low dose of MEA (100 mg/kg). Immediately after stress, plasma levels of GH and TSH increased; but this response was blocked by a high dose of MEA (300 mg/kg). MEA increased basal GH levels, but did not restore episodic GH, and lowered PRL in VMN/ ARC-lesioned animals. These results indicate that: (1) NE/EPI facilitate episodic GH and TSH release, (2) SRIF maintains low basal levels of GH and TSH, (3) MEA-induced PRL depletion does not involve DA systems and (4) MEA can be measured in tissue relatively simply using HPLC and electrochemical de

ISSN:0028-3835    

DOI:10.1159/000124221

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The effects of thyroid hormone deprivation and of subsequent replacement therapy on growth hormone (GH) secretion were investigated in unrestrained unanesthetized rats. Male rats were thyroparathyroidectomized (TPTX) 5 weeks prior to plasma sampling for GH assay, or to decapitation for evaluation of hypothalamic somatostatin (SRIF) content and in vitro SRIF and GH release. Thyroid hormone deprivation suppressed pulsatile GH secretion as well as GH release induced by clonidine (150 µg/kg). Treatment of TPTX rats with small doses of triiodothyronine (T3) restored an episodic pattern of GH secretion, but with lower peak values than controls, as well as the GH response to clonidine. Thyroid deprivation induced a 92-fold decrease in GH release from the pituitary; however, the ratio between GH release and GH content was similar in TPTX and normal rats, and human pancreatic growth hormone-releasing factor (GRF) (3 · 10–8M) was still able to stimulate residual GH release by hemipituitaries from TPTX rats in a manner similar to that in euthyroid controls (295 and 254% stimulation, respectively). Thyroid deprivation or T3 replacement did not modify SRIF content in the hypothalamus or other brain structures tested. The capacity of K+ depolarization to release SRIF in vitro from the hypothalamus was not modified by TPTX. These findings indicate that thyroid hormones are necessary to maintain both pulsatile and induced GH secretion in unanesthetized rats. In addition they suggest that impairment of GH secretion in thyroidectomized rats does not depend upon changes in the hypothalamic SRIF regulation of the hormone but could be dependent on a defect in GRF release and/or, most probably, GH synthesis directly at the pituitary le

ISSN:0028-3835    

DOI:10.1159/000124222

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Peptidyl-glycine α-amidation activity has been detected in human cerebrospinal fluid (CSF) and in several regions of the central nervous system. Activity was monitored by measuring conversion of mono-125I-D-Tyr-Val-Gly into mono-125I-D-Tyr-Val-NH2. The α-amidation activity in CSF is dependent on molecular oxygen, copper ions and ascorbic acid and appears to recognize a variety of peptide substrates which contain carboxyl terminal glycine residues. Kinetic analyses demonstrated Michaelis-Menten kinetics with a Km of 4.6 µM for D-Tyr-Val-Gly. The level of peptidyl-glycine α-amidation activity in 14 samples of CSF averaged 43 ± 5 pmol/ml/h (mean + SEM; range 11–85 pmol/ml/h) or 1.9 ± 0.2 pmol/mg protein/h. No difference was noted between samples from male and female subjects. Extracts of central nervous system tissue contained α-amidation activity. The highest levels of enzyme activity were found in the hypothalamus with lower levels in the neurohypophysis and the cerebral cortex. Still lower but detectable activity was found in the cerebellum and pons. Human peptidyl-glycine α-amidation activity is found in central nervous system tissues known to synthesize α-amidated neuropeptides and may be secreted from these tissues along with α-amidated peptid

ISSN:0028-3835    

DOI:10.1159/000124223

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The effect of indolamine derivatives on β-endorphin (β-end) release has been studied in vitro using rat anterior pituitary cells. Incubation of primary cultures for 2 h with 100 nmol/l of melatonin, serotonin or 5-methoxytryptamine significantly increased the β-end release in response to 20 nmol/l of ovine corticotropin-releasing factor (oCRF). Incubation of the cultures with 100 nmol/l of L-tryptophan, 5-hydroxy-L-tryptophan, 5-hydroxytryptophol or 5-methoxytryptophol had no effect on basal or CRF-induced β-end release. The effect of serotonin and melatonin was further tested in a superfusion system of dispersed rat anterior pituitary cells. Superfusion with oCRF (200 nmol/l) for 4 min elicited an immediate rapid increase in β-end release which lasted 30–40 min. Simultaneous superfusion with melatonin (1 µmol/l) or serotonin (1 µmol/l) significantly increased the effect of oCRF pulses on β-end release. We conclude that melatonin and serotonin are able to act directly on anterior pituitary cells to potentiate the effect of oCRF on β-e

ISSN:0028-3835    

DOI:10.1159/000124224

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

Immunoneutralization of endogenous gonadal steroids has recently been shown to modify pineal β-adrenoceptor function in intact Merino ewes. In the current study, interactions between gonadal steroids and these receptors have been further investigated. β-Adrenoceptor density and binding affinity both showed time-related changes in ewes; the significance of these changes requires further study. Two observations, firstly modification of β-adrenoceptor function by androstenedione and 17β-estradiol in ovariectomized, but not in intact ewes, and secondly that steroid-mediated effects on receptor density and binding affinity in the pineal of ovariectomized Merino ewes could be demonstrated during anestrus, but not during the breeding season for intact ewes, indicate that gonadal steroids may regulate pineal β-adrenoceptor variables in Merino ewes. It is suggested that gonadal steroids may regulate ovine pineal function in ewes, and that the seasonal differences in sensitivity of luteinizing hormone release to steroid feedback may be mediated in part via effects on the pineal g

ISSN:0028-3835    

DOI:10.1159/000124225

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The influence of the site of action of thyrotropin-releasing hormone (TRH) on the production of hyperglycemia was studied in rats by comparing the effectiveness of TRH administered by different routes. Administration of TRH (5 µg) into the lateral hypothalamus (LH) produced a hyperglycemia with a peak elevation of blood glucose of 140 mg/dl. Injection of 5 µg TRH into the ventromedial hypothalamus (VMH) produced a blood glucose elevation of 44 mg/dl, while injection of the same dose of TRH into the anterior hypothalamus (AH) produced a blood glucose elevation of 23 mg/dl. These findings indicate an LH site of action of TRH. Indeed, intra-LH administration of TRH (1–10 µg) caused dose-related increases in blood glucose. Administration of acetylcholine into the same site was also shown to induce hyperglycemia. The hyperglycemic effects of TRH and acetylcholine were antagonized by previous treatment of the LH site with atropine, a cholinergic receptor antagonist. Furthermore, the TRH-induced hyperglycemia was not observed or was greatly reduced in spinal rats or in adrenalectomized rats. The results indicate that TRH may act through the cholinergic receptor mechanisms within the LH region to induce hyperglycemia by promoting an increase in the sympathetic-adrenal medullary efferent acti

ISSN:0028-3835    

DOI:10.1159/000124226

出版商:S. Karger AG    

年代:1985

数据来源: Karger

摘要:

The basal activity of tuberoinfundibular dopaminergic (TIDA) neurons is higher and the response of these neurons to the stimulatory actions of prolactin is greater in the female than in the male rat. In the female rat, the restraint-stress-induced increase in serum prolactin concentrations is accompanied by a concurrent decrease in the activity of TIDA neurons. The purpose of the present study was to compare these effects of restraint in male and female rats. TIDA neuronal activity was estimated by measuring the rate of dopamine (DA) synthesis (DOPA accumulation after the administration of a decarboxylase inhibitor, NSD 1015) and the rate of DA turnover (decline of DA after administration of atyrosine hydroxylase inhibitor; α-methyltyrosine) in the median eminence. Thirty minutes of restraint increased serum prolactin concentrations in both male and female rats, but a greater response was observed in the females. Restraint also decreased the rates of synthesis and turnover of DA in the median eminence of the female but not the male rat. The difference in the response of TIDA neurons in male and female rats to restraint is not the consequence of neuronal differentiation resulting from neonatal androgen exposure, because restraint also decreased the activity of TIDA neurons in androgen-sterilized female rats. The inability of restraint stress to reduce TIDA neuronal activity in the male rat appears to be the consequence of testosterone, since TIDA neurons were responsive to restraint following castration of the males. In addition, the ability of restraint stress to decrease TIDA neuronal activity was inhibited in castrated male rats by pretreatment with testosterone, and was facilitate in intact male rats by estradiol pretreatment. Neither castration nor pretreatment with estradiol or testosterone altered the responsiveness of TIDA neurons to restraint in the female rat. These results suggest that male-female differences in the response of TIDA neurons to restraint stress is a consequence of the actions of testosterone in the male rat

ISSN:0028-3835    

DOI:10.1159/000124227

出版商:S. Karger AG    

年代:1985

数据来源: Karger