摘要:

Inthese three experiments, we investigated the effect of adrenalectomy and adrenal demedullation on the stress-induced impairment of long-term potentiation (LTP) in the rat hippocampal slice. In the first, adrenalectomy alone resulted in a significant reduction in LTP, while exposure to stress resulted in a further reduction. In the second, replacing corticosterone in adrenalectomized rats did not restore LTP. In the last experiment, demedullation resulted in a reduction in LTP similar to that induced by adrenalectomy, while exposure to stress did not result in a further reduction. In combination, these studies provide evidence that the adrenal medullary system modulates hippocampal plasticity and the stress-induced impairment of LTP.

ISSN:0028-3835    

DOI:10.1159/000125318

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

This study examined the effects of an alpha-2-adrenoceptor antagonist on the secretion of ACTH basally and in response to the opioid antagonist naloxone, which is known to stimulate ACTH secretion by an adrenergic mechanism. Eight normal men were given, in double-blind, random order, intravenous infusions of normal saline (placebo), idazoxan (alpha-2-adrenoceptor antagonist), naloxone and the combination of idazoxan and naloxone. Naloxone increased plasma ACTH and cortisol concentrations in comparison to placebo. Idazoxan significantly enhanced the ACTH and cortisol responses to naloxone but had no effect on plasma ACTH or cortisol concentrations when given alone. These findings suggest that during some conditions of increased ACTH secretion, inhibitory alpha-2-adrenoceptors are activated and that these receptors limit the ACTH response. This provides an explanation for some of the apparent contradictions in interpreting the data from previous studies on the effects of catecholamines on the secretion of ACTH.

ISSN:0028-3835    

DOI:10.1159/000125319

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The sleep in young adults with severe isolated growth hormone deficiency (IGHD) was examined by polysomnography. There was a significant decrease in delta sleep time (= stages 3 + 4, slow wave sleep, ‘deep sleep’), especially in stage 4. The total sleep time was significantly increased compared to age- and sex-matched normal subjects. The increase in total sleep time was related to an increase in stage 1 and stage 2 sleep. There was no significant difference in total rapid eye movement (REM) sleep time, but when correcting for the very long sleep time in the IGHD subjects, the cumulated REM time within the first 390 min of sleep was significantly less than in the normal subje

ISSN:0028-3835    

DOI:10.1159/000125320

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

Rats were treated with monosodium glutamate (MSG), 4 mg/g on alternate days for the first 10 days of life, to induce lesions of the arcuate nucleus and destroy the majority of growth hormone-releasing hormone (GHRH) neurones. At 10 weeks of age, control (n = 42) and MSG-treated (n = 36) male rats were used to test the effect of glucocorticoids on growth hormone (GH) secretion. Each treatment group was divided into six study groups to determine the effect of betamethasone (BM), administered either 3 or 20 h prior to sacrifice, alone and in combination with hypoglycaemia (insulin 0.1 U/100 g). BM treatment of male rats was without effect on plasma GH levels in control animals. In contrast, glucocorticoid administered either 3 h before sacrifice or the previous evening significantly reduced circulating GH (p < 0.001) in MSG-treated animals. The difference in plasma GH response to BM pretreatment in control rats and those with lesions of the arcuate nucleus indicates a hypothalamic action of glucocorticoids, presumably on somatostatin and GHRH neurones. In control animals the effects appear to be counterbalancing, but following destruction of GHRH neurones an uncompensated inhibitory influence was observed. Male MSG-treated rats had lower body weight (–25%) and reduced hypothalamic GHRH (–89%) and pituitary GH content (–69%) compared to male controls. Female rats which had undergone the same neonatal MSG treatment (n = 40) when sacrificed 1 week after their male counterparts showed similar reductions in body weight (–15%), hypothalamic GHRH (–74%), and pituitary GH (–67%). Interestingly, the hypothalamic concentration of GHRH in control female rats (n = 39) was only 41% of male controls, suggesting an important effect of sex hormones on GH

ISSN:0028-3835    

DOI:10.1159/000125321

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

To clarify the regulatory mechanisms for the secretion of somatostatin (SRIF) from the hypothalamus, the effects of intracerebroventricular (i.c.v.) administration of growth hormone-releasing factor (GRF) and corticotropin-releasing factor (CRF) on SRIF secretion into hypophysial portal blood were examined in pentobarbital-anesthetized male rats. Neither the concentration of SRIF in portal plasma nor the secretion rate of SRIF was changed after i.c.v. administration of 0.9% saline. Administration of 10 ng or 5 µg human GRF i.c.v. produced a significant increase in the portal plasma concentration and secretion rate of SRIF. Likewise, 5 µg CRF significantly increased the portal plasma concentration and secretion rate of SRIF. These results suggest that the neuropeptides GRF and CRF centrally influence SRIF secretion into hypophysial portal bloo

ISSN:0028-3835    

DOI:10.1159/000125322

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The role of the pituitary-adrenal axis on receptor binding and diurnal rhythmicity of benzodiazepines (BNZ) was assessed in the rat cerebral cortex. Groups of intact, adrenalectomized (ADx) and/or hypophysectomized (HPx) rats were killed at six different time intervals during the 24-hour cycle. BNZ binding was estimated by Scatchard analysis of 3H-flunitrazepam high-affinity binding to rat cerebral cortex. Intact and sham ADx animals show a similar pattern in diurnal thythm of BNZ binding, with a maximal concentration at midnight. Bilateral ADx induced a significant increase in Bmax at all time intervals studied, the largest rise appearing at midnight. HPx alone led to a slightly smaller rise in Bmax than in ADx rats, while HPx performed in ADx rats did not modify the response to ADx alone. Bmaχ of BNZ binding in ADx rats reached maximal values at 3–7 days after surgery, and decreased somewhat at 15 days post-ADx. Corticosterone administration at a single dose of 5 mg i.p. 24 h before sacrifice returned Bmax to normal values in ADx as well as in ADx plus HPx rats. The corticosterone effect is not exerted on the BNZ binding sites themselves, as revealed by the lack of effect of this glucocorticoid in vitro. These findings indicate that BNZ receptors in rat cerebral cortex can be modified by the adrenal gland, with corticosterone as a primary effect

ISSN:0028-3835    

DOI:10.1159/000125323

出版商:S. Karger AG    

年代:1990

数据来源: Karger

摘要:

The concentration of β-endorphin-immunoreactivity (βE-IR) in cerebrospinal fluid (CSF) and plasma of rats was determined following intracerebroventricular (ICV) treatment of conscious animals with substances known to stimulate the release of βE and other pro-opiomelanocortin (POMC)-derived peptides at the level of the anterior and intermediate lobes of the pituitary. The β-adrenoceptor agoinst isoproterenol (ISO) did not influence the concentration of βE-IR in CSF collected 5–60 min after ICV administration of doses ranging from 3 to 30,000 pg/rat. Plasma βE-IR levels, however, were significantly increased 20 min following ICV injection of 30,000 pg ISO. ICV treatment of animals with ovine corticotropin-releasing factor (CRF; 30–30,000 pg/rat) also did not affect CSFlevels of βE-IR, whereas CRF in a dose of 30 pg significantly decreased, and in doses of 300–30,000 pg enhanced plasma βE-IR concentrations as determined by 20 min following treatments. ICV injection of arginine8-vasopressin (AVP) in doses of 10–1,000 pg/rat dose-dependently elevated the βE-IR concentration in CSF without affecting plasma βE-IR levels. This AVP-induced increase in CSF βE-IR was maximal 20–35 min and βE-IR levels had returned to basal 60 min following treatment. The data indicate that AVP and not ISO and CRF is a stimulator of CSF levels of βE-IR. As βE-IR in CSF likely originates from brain POMC neurons, these results suggest the hot vasopressin may be a physiological regulator of brain POMC activity, and may act as a releasing factor for POMC-derive

ISSN:0028-3835    

DOI:10.1159/000125324

出版商:S. Karger AG    

年代:1990

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000125325

出版商:S. Karger AG    

年代:1990

数据来源: Karger