ISSN:0028-3835    

DOI:10.1159/000123318

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

To evaluate the role of cholinergic neurones within the hypothalamus in modulating pancreatic-endocrine function, plasma levels of glucagon, insulin and glucose were measured after microinjection of acetylcholine into the ventromedial hypothalamic nucleus (VMH) of rabbits. Injection of acetylcholine (5 × 10–8 mol in 2 µl of saline) into the VMH of unanesthetized, unrestrained animals resulted in a prompt elevation of immunoreactive glucagon and glucose levels without any significant change in immunoreactive insulin level. The suppression of insulin secretion following cholinergic stimulation of the VMH was not counteracted by intravenous infusion of glucose (0.25 g/kg). Bilateral adrenalectomy prevented both hyperglucagonemia and hyperglycemia induced by the acetylcholine injection into the VMH. In adrenalectomized rabbits, exogenous glucose load was followed by a significant rise in the plasma insulin level despite the hypothalamic injection of acetylcholine. However, the response of insulin release to glucose load in these animals was much less than in adrenalectomized, saline-treated, control animals. These data support the conclusion that the action of acetylcholine within the hypothalamus on the pancreatic hormone secretions is mediated to a large part through sympatho-adrenomedullary activity. However, a part of the decreased insulin response to glucose may be mediated by direct innervation of the pancr

ISSN:0028-3835    

DOI:10.1159/000123319

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Estradiol (E)-filled Silastic capsules were implanted subcutaneously to characterize the estrogen stimulus sufficient to initiate cyclic LH secretion in female rats ovariectomized on diestrus 1 of the estrous cycle. Such capsules elevate preoptic area, hypothalamic and hypophysial cell nuclear estrogen receptor levels to proestrous values within ½ h following insertion; upon removal of the capsules, nuclear receptor levels decline monotonically to ovariectomized control levels by 8 h in brain and 12 h in pituitary. Three parameters of the E stimulus were studied:latent period, duration, and continuity. E stimuli, short in duration (7–12 h) and discontinuous in nature (3 h pulses 12 or 15 h apart), effectively stimulated LH surges on ‘proestrus’. However, these stimuli had to begin 30 h prior to the onset of LH release. Such a latent period for estrogen action was not observed when we monitored the ability of the same E stimuli to enhance pituitary responsiveness to GnRH. These studies demonstrate that the ‘rate-limiting step’ for estrogen’s positive feedback action is located within the estrogen-sensitive brain circuits controlling GnRH release and defines the temporal characteristics of E stimuli activating th

ISSN:0028-3835    

DOI:10.1159/000123320

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

The effect of the serotonin-releasing drug parachloroamphetamine (PCA) on plasma renin activity was studied in rats 4 days after surgical lesions of the mediobasal hypothalamus, anterolateral deafferentation of the mediobasal hypothalamus, posterolateral deafferentation, or hypophysectomy. PCA increased plasma renin activity in sham-operated rats, but it failed to increase plasma renin activity in rats with mediobasal hypothalamic lesions or posterolateral deafferentation. The response to PCA was unaffected by anterolateral deafferentation and enhanced by hypophysectomy. There were no significant differences in plasma renin activity in lesioned, deafferented, and hypophysectomized rats injected with saline. The data indicate that the mediobasal hypothalamus is part of the pathway by which central serotonergic neurons affect renin secretion, and that the effect is not mediated via hormones of the pituitary gland.

ISSN:0028-3835    

DOI:10.1159/000123321

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Characterization of the molecular, immunological and biological properties of a thyrotropin-stimulating hormone (TSH)-like peptide in rodent brain tissue showed similarities to its pituitary counterpart. The distribution of immunoreactivity in rodent brain was determined by radioimmunoassay in both intact and hypophysectomized animals. Easily detectable but smaller quantities of immunoassayable TSH were present in formalin fixed, acetone-stored brains from Macaca mullata. No change in the level of this TSH-like peptide was observed in most rat brain parts, although the hypothalamus did show a significant drop in hormone level after removal of the pituitary. Extracts of brain containing TSH-like material restored thyroid histology to normal when administered to hypophysectomized rats. Tissue cultured neural cells from both intact and hypophysectomized rats released a TSH-like material into the medium over a 30-day time period. Sodium /-thyroxine suppressed TSH release from pituitary monolayers but did not alter TSH release from brain derived cells that were similarly cultured. Surgical thyroidectomy resulted in a striking rise in serum TSH concentrations with no alteration in the content of brain TSH.

ISSN:0028-3835    

DOI:10.1159/000123322

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Two experiments were conducted to identify sites in the female rat brain at which dihydrotestosterone acts to inhibit estradiol-induced feminine sexual behavior. 27 gauge cannulae containing either crystalline dihydrotestosterone propionate (DHTP) or cholesterol were implanted unilaterally into the lateral septum, preoptic area-anterior hypothalamic area, ventromedial nucleus of the hypothalamus or caudate putamen. In experiment 1, rats were given stereotaxic implants of steroids prior to being injected daily with estradiol benzoate (EB; 0.5 µg/100 g body weight) and tested for sexual receptivity. In experiment 2, animals were injected daily with EB (0.9 µg/100 g body weight) and tested for sexual receptivity prior to and after stereotaxic implantation of steroids. In both experiments significant reductions in lordotic behavior were obtained only with lateral septal implants of DHT

ISSN:0028-3835    

DOI:10.1159/000123323

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

Bromocriptine treatment of patients with invasive prolactin (PRL)-secreting pituitary adenomas does not invariably result in normalization of the plasma PRL levels. We previously showed that the antiestrogenic drug tamoxifen inhibited hormone release from transplantable PRL-secreting pituitary tumors in rats. In 8 patients with invasive PRL-secreting pituitary adenomas with extrasellar extension, the effect of the administration of tamoxifen was investigated on the plasma PRL concentration and on the bromocriptine-mediated inhibition of PRL release. Treatment for 5 days with tamoxifen (20 mg/day) suppressed plasma PRL levels as measured in 5 samples over the day significantly by 20 ± 3% (means ± SEM; p < 0.01). During tamoxifen administration the inhibition of PRL secretion by 2.5 mg bromocriptine was further suppressed by 36 ± 7%, in comparison with the plasma PRL levels after bromocriptine alone (p < 0.0

ISSN:0028-3835    

DOI:10.1159/000123324

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

The pharmacologic effects of intravenous melatonin on hypothalamic-adenohypophyseal function were studied in male rhesus monkeys (n = 10) and compared to control animals (n = 9–13). Basal and arginine- or L-dopa-stimulated values of growth hormone in melatonin-treated animals were similar to those of control primates. Insulin-stimulated growth hormone secretion was slightly decreased. Melatonin did not affect basal or thyroid stimulating hormone releasing hormone (TRH)-stimulated values of thyroid stimulating hormone (TSH) or prolactin. No effects were seen on basal and gonadotropin releasing hormone (GnRH)-stimulated luteinizing hormone (LH) or follicle stimulating hormone (FSH) secretio

ISSN:0028-3835    

DOI:10.1159/000123325

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

In the present study the effect of methadone (M) on gonadotropin-releasing hormone in the rat hypothalamus was investigated. The specificity of the M effect was demonstrated by injecting M (100 ng) and the M antagonist, naloxone (5 ng), into the ventromedial hypothalamus. A significant drop in the blood testosterone level (p < 0.05) 15 min following M injection and reversal following naloxone administration suggest a decrease in synthesis or release of LHRH. To determine whether the LHRH response to dopamine (DA) is altered by M, studies were conducted in vitro and in vivo. For the in vitro study hypothalami were incubated with M (10–7 M), DA (10–7 M), DA plus M, and DA plus M plus naloxone. Supernatants from the incubate were used to coincubate pituitaries in order to study the effect on luteinizing hormone release. Treatment of the hypothalamus with M had no effect on basal but inhibited the DA-stimulated release of LHRH. For the in vivo study rats were pretreated with decarboxylase inhibitor (RO4–4602) followed by treatment per kilogram body weight with M (10 mg), L-dopa (1, 10, and 100 mg), L-dopa plus M, LHRH (500 ng), and M plus LHRH. M had no effect on the LHRH-induced increase in testosterone levels, whereas the L-dopa-induced increase in testosterone was blunted by M treatment. It is concluded that M blocks the DA-mediated release of gonadotropin-releasing hormone in the rat hypotha

ISSN:0028-3835    

DOI:10.1159/000123326

出版商:S. Karger AG    

年代:1982

数据来源: Karger

摘要:

This study was to ascertain the effect of naloxone and dexamethasone on vasopressin and β-endorphin release in the rat during inescapable electric foot shock stress. Plasma vasopressin concentrations were not affected by electric foot shock in vehicle-treated rats, but were raised significantly by the stress in animals pretreated with naloxone. The stress-induced increase in plasma β-endorphin-like immunoreactivity (β-EI) was similar whether the rats had received naloxone or not. Plasma β-EI consisted of equal amounts of β-endorphin-like and β-lipotropin-like material as revealed by gel filtration. Dexamethasone almost abolished the foot shock-induced increase in plasma β-EI and, in the presence of dexamethasone, stress was now effective in elevating plasma vasopressin concentrations. These results are consistent with the hypothesis that β-endorphin, released from the anterior pituitary, inhibits the release of vasopressin from the posterior lobe of the pituitary gland during foot shock-induced

ISSN:0028-3835    

DOI:10.1159/000123327

出版商:S. Karger AG    

年代:1982

数据来源: Karger