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Titolo:
EXOGENOUS GLUTAMATE ENHANCES GLUTAMATE-RECEPTOR SUBUNIT EXPRESSION DURING SELECTIVE NEURONAL INJURY IN THE VENTRAL ARCUATE NUCLEUS OF POSTNATAL MICE
Autore:
HU LM; FERNSTROM JD; GOLDSMITH PC;
Indirizzi:
UNIV CALIF SAN FRANCISCO,DEPT OBSTET GYNECOL & REPROD SCI,CTR REPROD ENDOCRINOL SAN FRANCISCO CA 94143 UNIV CALIF SAN FRANCISCO,DEPT OBSTET GYNECOL & REPROD SCI,CTR REPROD ENDOCRINOL SAN FRANCISCO CA 94143 UNIV PITTSBURGH,SCH MED,DEPT PSYCHIAT PITTSBURGH PA 00000 UNIV PITTSBURGH,SCH MED,DEPT PHARMACOL PITTSBURGH PA 00000 UNIV PITTSBURGH,SCH MED,DEPT NEUROSCI PITTSBURGH PA 00000
Titolo Testata:
Neuroendocrinology
fascicolo: 2, volume: 68, anno: 1998,
pagine: 77 - 88
SICI:
0028-3835(1998)68:2<77:EGEGSE>2.0.ZU;2-W
Fonte:
ISI
Lingua:
ENG
Soggetto:
FIBRILLARY ACIDIC PROTEIN; METHYL-D-ASPARTATE; BRAIN; CELLS; RELEASE; DEATH; EXCITOTOXICITY; HYPOTHALAMUS; LOCALIZATION; ASTROCYTES;
Keywords:
MONOSODIUM GLUTAMATE; ARCUATE NUCLEUS; MEDIAN EMINENCE; NEURODEGENERATION; APOPTOSIS; NECROSIS; GLUTAMATE RECEPTOR; TYROSINE HYDROXYLASE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Science Citation Index Expanded
Citazioni:
41
Recensione:
Indirizzi per estratti:
Citazione:
L.M. Hu et al., "EXOGENOUS GLUTAMATE ENHANCES GLUTAMATE-RECEPTOR SUBUNIT EXPRESSION DURING SELECTIVE NEURONAL INJURY IN THE VENTRAL ARCUATE NUCLEUS OF POSTNATAL MICE", Neuroendocrinology, 68(2), 1998, pp. 77-88

Abstract

Administration of high doses of glutamate (GIu) leads to selective neurodegeneration in discrete brain regions near circumventriclular organs of the early postnatal mouse. The arcuate nucleus-median eminence complex (ARC-ME) appears to be the most Glu-sensitive of these brain regions, perhaps because of the intimate relationships between its neurons and specialized astroglial tanycytes. To investigate the mechanism of Glu-induced neuronal loss, we administered graded doses of the sodium salt of glutamate (MSG) to postnatal mice, measured their plasma Glu concentrations, and performed microscopic analyses of the ARC-ME region 5 h after treatment. Nursing, 7-day-old mouse pups (CD1, Charles River, Hollister, Calif.) were injected subcutaneously with single doses of 0.1-0.5 or 1.0-4.0 mg of MSG per g BW, or with water vehicle alone. Mice were decapitated 5 h later and the brains immediately fixed byimmersion in buffered aldehydes. Frontal vibratome tissue sections atcomparable levels of the ARC-ME were examined by light microscopy. A dose of 4.0 mg MSG/g BW caused neurodegeneration throughout the ARC region, while 1.0 mg/g MSG resulted in less extensive damage. Injection of 0.2 mg MSG/g BW, which raised plasma Glu concentrations 17-fold after 15 min, was the minimum dose tested at which nuclear and cytoplasmic changes were observed in a small group of subependymal neurons near the lateral recesses of the third ventricle. Higher doses of 0.3-0.5 mg MSG caused injury to additional neurons situated farther laterally, but damage remained confined to the ventral region of the ARC nucleus. Ultrastructural examination showed some subependymal neurons with pyknotic nuclei, reduced cytoplasmic volume, and swollen subcellular organelles, while others had fragmented and condensed nuclear material. Immunostaining for tyrosine hydroxylase indicated that dopamine neurons were spared at the threshold dose, but suffered damage after higher doses of MSG. Immunostaining for Glu receptor subtypes revealed that 0.2mg MSG/g BW enhanced neuronal expression of NMDAR1 and of GluR2/4, and that higher doses of MSG preferentially increased NMDAR1 expression in injured neurons. These results extend previous reports of Glu sensitivity in the ARC-ME region of 7-day postnatal mice. A dose of 0.2 mg MSG/g BW s.c. causes clear but discrete injury to specific subependymal neurons of undetermined phenotype near the base of the third ventricle. Slightly higher doses of MSG evoke damage of additional neurons confined to the ventral region of the ARC traversed by tanycytes. These same greater amounts of MSG promote dose-related increase in the expression of NMDAR1 more than of GluR2/4 in injured ARC neurons, suggesting that elevated GIu receptor levels may contribute to or be related toneuronal cell death. Taken together with previous findings, the data suggest that GIu responsitivity in the ARC-ME of the postnatal mouse may result from transient developmental conditions involving the numerical ratios and juxtaposition between tanycytes and neurons, expressionof Glu receptors, and perhaps other ontogenetic factors which may notpersist in the mature adult.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 30/09/20 alle ore 11:53:22