Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01189 (beta-endorphin)
 21,003 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Monosodium glutamate (MSG) treatment of neonatal rats results in degenerative lesions of the medial basal hypothalamus, particularly the arcuate nucleus (AN). The AN is rich in corticotropin-releasing hormone (CRF) and adrenocorticotrophic hormone/alpha-melanocyte-stimulating hormone (alpha-MSH). These substances are part of a negative feedback mechanism for the regulation of interleukin-1 (IL1), a cytokine with diverse biologic actions including a role in sleep regulation. The purpose of these experiments was to determine the effects of exposure of neonatal rats to MSG on their responsiveness as adults to IL1. Adult rats, treated as neonates with MSG or the saline, were injected intracerebroventricularly during the light phase with three doses of IL1 (2.5, 10.0, 25.0 ng) and sleep-wake activity determined and brain temperature recorded for the next 6 hr. IL1 administration induced fever in both treatment groups at each dose of IL1 tested, and the febrile response of the MSG rats to the 25.0 ng dose of IL1 was greater than that of the saline control rats. In saline-treated rats, the 2.5 ng dose of IL1 enhanced non-rapid-eye-movement sleep (NREMS) without affecting rapid-eye-movement sleep (REMS) or wakefulness, whereas the 25.0 ng dose of IL1 inhibited both NREMS and REMS. In contrast, only the 10.0 ng dose of IL1 altered NREMS in MSG-treated rats. These results support the hypothesis that CRF- and alpha-MSH-containing perikarya are involved in regulation of IL1 actions.
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PMID:Responsiveness of rats to interleukin-1: effects of monosodium glutamate treatment of neonates. 217 94

Monosodium glutamate (MSG) was given to neonatal male rats to determine its effects on neurons containing beta-endorphin (beta-END) and alpha-melanocyte stimulating hormone (alpha-MSH) within the basal hypothalamus (arcuate nucleus) and caudal medulla [nucleus tractus solitarius (NTS)] and on the levels of beta-END and alpha-MSH within these areas. Immunocytochemical studies demonstrated a reduction in the number of cells within the medial hypothalamic area (arcuate nucleus) among MSG-treated animals versus saline controls. MSG did not reduce the number of cell bodies within the caudal medulla (NTS). MSG significantly reduced beta-END and alpha-MSH immunoreactive levels in the basal hypothalamus as determined by radioimmunoassay. Whereas a significant reduction in the level of beta-END occurred in the ventral caudal medulla (VCM), none occurred in the dorsal caudal medulla (DCM). In contrast, levels of alpha-MSH increased significantly in the DCM among animals receiving MSG compared to control animals. This study documents the contribution of beta-endorphin containing neurons of the basal hypothalamus to areas of the caudal medulla. The effect of MSG on beta-endorphin and alpha-MSH neurons in these areas and their differential effects on levels in the caudal medulla areas raises questions about the sites of origin of these peptides.
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PMID:MSG effects on beta-endorphin and alpha-MSH in the hypothalamus and caudal medulla. 285 57

Alterations of the sleep-wake cycle have been studied in male adult rats after neonatal administration of monosodium glutamate (MSG; 4 X 4 mg/g body wt.). Results indicated that MSG treatment caused: an almost complete disappearance of ACTH and alpha-MSH immunoreactive (IR) perikarya in the rostral part of the arcuate nucleus; an increase in total sleep duration with a more pronounced effect on paradoxical sleep. Regarding circadian rhythmicity there was a trend to a decomposition of the 24 h period into ultradian components (12 h, 8 h, 6 h harmonics). The participation of pro-opiomelanocortin peptides in sleep regulation is discussed.
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PMID:Neonatal monosodium glutamate dosing alters the sleep-wake cycle of the mature rat. 301 98

Mice treated neonatally with MSG (4 mg/g) were compared to saline-injected controls on a number of neurochemical parameters of brainstem noradrenergic activity. MSG treatment resulted in an attenuation of brainstem norepinephrine (NE) decline after alpha-methyl-p-tyrosine administration. Neonatal MSG administration did not result in alterations in the steady state levels of brainstem NE or MOPEG. The synthesis of NE was slightly increased in the pons-medulla of MSG-treated mice as indexed by pargyline-induced NE accumulation. NE release, however, appeared diminished as reflected by a significant (p less than 0.05) decrease in the ratio of normetanephrine to NE found in the pons-medulla of MSG-treated mice given pargyline. The results suggest that MSG-induced damage to the arcuate nucleus produces selective alterations in brainstem NE systems. These alterations may reflect the toxic action of MSG on the opiomelanocortin neurons of the arcuate nucleus or other descending systems that are damaged by MSG. The loss of the descending opiomelanocortin input to the brainstem could result in these types of neurochemical consequences since the pharmacologic action of opiate drugs results in a selective enhancement of brainstem NE turnover in rodents.
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PMID:Neonatal monosodium glutamate administration alters noradrenergic measures in the brainstem of the mouse. 404 24

Neurotoxic doses of monosodium glutamate were administered to neonatal male and female Sprague-Dawley rats for five days postpartum. The rats were tested at 6 months for alterations in two forms of activity--initial activity in an open field and overnight activity in a familiar cage. In comparison with age-, sex- and handling-matched littermate controls, experimental subjects exhibited increased open field behaviors and reduced overnight activity. Subsequent histology indicated marked reductions in arcuate and periarcuate cells which included but probably were not limited to beta-endorphin containing neurons. These findings indicate that neonatal MSG has long-term behavioral and neurological consequences, that some changes occur within behaviorally discrete systems, and that they may be associated with functional alterations within endogenous opioid systems, inter alia.
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PMID:Neonatal monosodium glutamate differentially alters two models of behavioral activity in conjunction with reduced hypothalamic endorphins. 631 4

In the present investigation, it was found that the number of beta-endorphin (beta-END)-immunoreactive neurons of hypothalamic arcuate nucleus (ARC) in MSG-treated rats decreased by 60.7%. No significant differences in the baseline pain threshold and the baseline corticosterone (CS) level were observed between the MSG-treated group and the control group. After electrical foot shock for 30 min, the analgesia effect was decreased significantly (P < 0.001) in MSG-treated rats, while the CS levels of both MSG-treated rats and control rats were increased remarked (P < 0.01). The results suggest that the beta-END neurons of ARC were involved in analgesia, but not in CS reaction during stress.
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PMID:[The analgesia effect and plasma corticosterone reaction during stress in adult rats treated neonatally with monosodium glutamate]. 797 3

The effect of neonatal treatment with monosodium L-glutamate (MSG) on the dopaminergic systems of the medial basal hypothalamus has been investigated using tyrosine hydroxylase (TH) and aromatic L-amino acid decarboxylase (AADC) immunocytochemistry. Changes in plasma levels of prolactin (PRL) and alpha-melanocyte-stimulating hormone (MSH) have also been determined in intact and in MSG-treated rats after inhibition of TH by alpha-methyl-p-tyrosine (alpha-MpT) or without inhibition of enzyme activity. Monosodium glutamate resulted in a 40% reduction in the number of TH immunopositive tuberoinfundibular neurons, but no change in the number of AADC-positive tuberoinfundibular nerve cells, indicating that this reduction has occurred mainly in TH-positive but AADC-negative elements, i.e., in L-DOPA-ergic neurons. In contrast, MSG did not cause changes in the number of TH and AADC immunoreactive neurons of the periventriculohypophysial and tuberohypophysial dopaminergic systems, and it did not influence basal plasma PRL levels. alpha-methyl-p-tyrosine has increased plasma PRL concentrations in both control and MSG-treated rats of both sexes, but significantly higher responses were detected in females. None of the treatments had any effect on plasma MSH level. These findings suggest that MSG affects primarily L-DOPA-ergic neurons located in the ventrolateral part of the arcuate nucleus, but not dopaminergic neurons situated in the dorsomedial part of the arcuate nucleus; neither PRL nor MSH secretion is altered by MSG; a significant sex difference exists in the pituitary PRL response to inhibition of TH, and this response is not affected by MSG.
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PMID:Effect of neonatal treatment with monosodium glutamate on dopaminergic and L-DOPA-ergic neurons of the medial basal hypothalamus and on prolactin and MSH secretion of rats. 1159 61

In the present study, newborn male Wistar rats were injected, subcutaneously, five times, every other day, with monosodium glutamate (MSG, 4 g/kg bw) or saline (as control, C), during the neonatal period. MSG animals developed destruction of the arcuate nuclei (ARC) with absence of NPY-immunoreactive cell bodies, which impaired both the food intake (baseline) and the 2-deoxy-D-glucose (2DG) glucoprivic feeding response. Increases in the immunoreactivity of corticotropin-releasing hormone-cell bodies in the paraventricular nuclei might have developed to compensate for the atrophy of the pituitary in MSG-treated rats. After systemic 2DG injection, neither the C nor the MSG rats increased their food intake, but they showed similar hyperglycemic responses, whereas plasma free fatty acids (FFA) increased only in the C group. In other groups, 2DG, norepinephrine (NE), neostigmine (NEO) and saline were intracerebroventricularly (i.c.v.) administered. In this condition, impairment of the hyperglycemic and food intake responses, associated to a lower increase in plasma FFA levels, were observed. As opposed to this, the MSG treatment gives support to NE effects, enhancing food intake, as well as plasma glucose and FFA levels. After NEO, plasma glucose increased only in the MSG group, while plasma FFA levels were elevated in the C rats. Taken together, the results obtained after MSG treatment point to a separate neural control of the hyperglycemic response and of the lipid mobilization when stimulated by central 2DG, NE or NEO administration. It seems likely that the excitatory neural pathway that controls lipid metabolism and is present in C rats was destroyed by the MSG treatment.
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PMID:Central but not peripheral glucoprivation is impaired in monosodium glutamate-treated rats. 1640 10