摘要:

Monosodium glutamate (MSG) has been shown to alter several neuroendocrine functions in neonatally treated rats. To evaluate for possible alterations in the hypothalamic-pituitary-adrenal axis, we injected rats during the neonatal period with MSG or saline (controls). An increase in basal plasma corticosterone levels associated with a blunted circadian variation was observed. Ether exposure produced a significant elevation in plasma corticosterone concentration in both groups of animals. However, while the increase in controls was 181.3% for male and 193.9% for female rats, in the MSG-treated rats it was only 60.7 and 31.6%, respectively. The intraperitoneal administration of high dexamethasone doses blocked corticosterone secretion in both groups. However, whereas the lowest dose (0.10 µg/kg) suppressed corticosterone secretion in control animals, it was ineffective in MSG-treated rats. The morphological study of adrenals revealed signs of a hyperfunctional state in MSG-treated rats. These data suggest that the central lesions produced by MSG treatment disrupt the regulation of the hypothalamic-pituitary-adrenal axis

ISSN:0028-3835    

DOI:10.1159/000125076

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The purpose of this study was to compare the control of adrenocorticotropin (ACTH) and corticosterone secretion in homozygous Brattleboro rats with their syngeneic controls, Long-Evans rats, and with rats of the Wistar strain. Plasma concentrations of ACTH and corticosterone were measured by radioimmunoassay in trunk blood, and corticotropin-releasing factor 41 (CRF-41), arginine vasopressin (AVP), and oxytocin were assayed in hypophysial portal vessel blood. Portal plasma was extracted with methanol for CRF-41 determination, and four different antisera and several different high-performance liquid chromatography (HPLC) systems were used to investigate AVP release. The peripheral plasma concentrations of ACTH and corticosterone were significantly higher in Long-Evans and homozygous Brattleboro than in Wistar rats. This difference was due, at least in part, to an approximately twofold greater release of CRF-41 into hypophysial portal blood of the Long-Evans and Brattleboro compared with Wistar rats. There was no significant difference between the strains in the output of oxytocin into portal blood. While no AVP could be detected in the neural lobe of homozygous Brattleboro rats, a small amount of AVP-like immunoreactivity was detected in unextracted hypophysial portal blood from homozygous Brattleboro rats. However, this AVP-like immunoreactivity was clearly distinct from authentic AVP in several HPLC systems, had no antidiuretic activity, and on gel filtration had a relative molecular mass greater than 5 kD. In contrast, the AVP-like immunoreactivity in hypophysial portal blood from Long-Evans rats co-eluted with authentic AVP in all HPLC systems tested. These findings show that in the homozygous Brattleboro rat authentic AVP is not released into hypophysial portal blood and that, therefore, the normal plasma concentrations of ACTH in this mutant are maintained by CRF-41 and possibly other hypothalamic and/or pituitary factors which facilitate ACTH release.

ISSN:0028-3835    

DOI:10.1159/000125077

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The effect of U50488H, a potent opioid K-receptor agonist, was investigated on the urine volume and on the secretion of arginine vasopressin (AVP) in response to dehydration or hyperosmolar or hypovolemic stimulation in conscious rats. This agonist markedly increased the urine volume in normally hydrated rats and suppressed plasma AVP in a dose-dependent manner in rats given hyperosmolar saline. This suppression of plasma AVP was completely reversed by concurrent injection of naloxone. U50488H also inhibited the release of AVP in dehydrated or hypovolemic rats. These findings indicate that the diuresis induced by U50488H is mainly caused by the suppression of plasma AVP. They also suggest that the K-opioid receptor plays an important role in regulating the secretion of AVP.

ISSN:0028-3835    

DOI:10.1159/000125078

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

The roles of prolactin (PRL) and the ovarian hormones, estradiol and progesterone, in the control of tuberoinfundibular dopaminergic neurons of aged female rats were investigated. The in situ molar activity of tyrosine hydroxylase (TH) in neurites of these neurons was assayed by measuring the rate of accumulation of L-dihydroxyphenylalanine in the median eminence following the administration of a L-dihydroxiphenylalanine decarboxylase inhibitor. The TH mass was measured by an immunoblot assay using rat TH as the standard. Pituitary implants in aged ovariectomized animals resulted in a significant increase in the median eminence of both the mass and in situ molar activity of TH. When circulating PRL of aged rats was neutralized by administration of antiserum against rat PRL, the activity of TH was reduced significantly compared to that of animals treated with preimmune serum. In aged ovariectomized rats treated with both estradiol and progesterone, the in situ molar activity of TH increased significantly compared to animals treated only with the solvent vehicle, estradiol, or progesterone. The stimulatory effect of estradiol and progesterone appeared to be mediated through a mechanism that did not involve PRL, since neutralization of circulating PRL failed to prevent an increase in TH activity in estradiol-progesterone-treated animals. None of these treatments affected the in situ activity of TH in the superior cervical ganglion. We conclude that PRL as well as combined estradiol-progesterone treatment have important roles in the maintenance of TH activity in aged tuberoinfundibular dopaminergic neurons.

ISSN:0028-3835    

DOI:10.1159/000125079

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Neurohypophyseal secretion of oxytocin (OT) in response to dehydration, hypovolemia, restraint, and parturition in rats is known to be potentiated by the opioid antagonist naloxone. The present studies demonstrated that stimulation of OT secretion by systemic injections of cholecystokinin (CCK) and lithium chloride (LiCl) likewise are potentiated by naloxone pretreatment. Moreover, the inhibitory effects of CCK and LiCl on gastric motility and feeding similarly were enhanced by naloxone. Because neurohypophyseal hormone secretion and inhibition of gastric motility are known to be mediated by oxytocinergic neurons projecting from the paraventricular nucleus of the hypothalamus, this parallel potentiation by naloxone of CCK- and LiCl-induced effects on OT secretion, gastric motility, and food intake suggests that one of the pathways involved in the central control of feeding behavior also may be oxytocinergic. These findings therefore provide evidence in support of an important role of endogenous opioid peptides in regulating OT secretion in a diffuse neuronal system that mediates an integrated neuroendocrine, autonomic, and behavioral response to CCK, LiCl, and perhaps other treatments that similarly affect ingestive behavior in rats.

ISSN:0028-3835    

DOI:10.1159/000125080

出版商:S. Karger AG    

年代:1988

数据来源: Karger

摘要:

Corticotropin-releasing factor (CRF) is localized in fibers in the noradrenergic nucleus locus ceruleus (LC) and alters LC discharge characteristics when administered centrally. To determine whether CRF functions as a neurotransmitter in the LC during stress, the effects of hemodynamic stress on LC discharge were compared to those of CRF. Hemodynamic stress elicited by intravenous nitroprusside infusion produced identical effects on LC spontaneous and sensory-evoked discharge as those reported for centrally administered CRF. Thus, nitroprusside increased LC spontaneous discharge rates, and disrupted LC discharge evoked by sensory stimuli such that the stimuli were less effective in producing phasic increases in LC discharge. The neuronal effects of nitroprusside were completely blocked by central administration of the CRF receptor antagonist, α helical CRF9–41, but not by pretreatment with dexamethasone which blocks stress-elicited hypophyseal CRF release. The present results confirm other reports of LC activation by stressors, and extend these studies by demonstrating that, in certain circumstances, this activation is dependent on endogenous CRF. This study supports the concept that CRF functions as a neurotransmitter in the LC in the initiation of stress respons

ISSN:0028-3835    

DOI:10.1159/000125081

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000125082

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000125083

出版商:S. Karger AG    

年代:1988

数据来源: Karger

ISSN:0028-3835    

DOI:10.1159/000125065

出版商:S. Karger AG    

年代:1988

数据来源: Karger