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Titolo:
Ethanol pre-exposure suppresses HIV-1 glycoprotein 120-induced neuronal degeneration by abrogating endogenous glutamate/Ca2+-mediated neurotoxicity
Autore:
Belmadani, A; Zou, JY; Schipma, MJ; Neafsey, EJ; Collins, MA;
Indirizzi:
Loyola Univ, Stritch Sch Med, Dept Cell Biol Neurobiol & Anat, Div Biochem, Maywood, IL 60153 USA Loyola Univ Maywood IL USA 60153 Anat, Div Biochem, Maywood, IL 60153 USA
Titolo Testata:
NEUROSCIENCE
fascicolo: 3, volume: 104, anno: 2001,
pagine: 769 - 781
SICI:
0306-4522(2001)104:3<769:EPSHG1>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
COAT PROTEIN GP120; RECEPTOR-MEDIATED NEUROTOXICITY; ENVELOPE PROTEIN; ARACHIDONIC-ACID; SLICE CULTURES; EXTRACELLULAR GLUTAMATE; TRANSGENIC MICE; NERVOUS-SYSTEM; CELL-CULTURES; NITRIC-OXIDE;
Keywords:
excitotoxicity; brain damage; organotypic; brain slice; arachidonic acid; astroglia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
64
Recensione:
Indirizzi per estratti:
Indirizzo: Collins, MA Loyola Univ, Stritch Sch Med, Dept Cell Biol Neurobiol & Anat,Div Biochem, 2160 S 1st Ave, Maywood, IL 60153 USA Loyola Univ 2160 S 1st Ave Maywood IL USA 60153 , IL 60153 USA
Citazione:
A. Belmadani et al., "Ethanol pre-exposure suppresses HIV-1 glycoprotein 120-induced neuronal degeneration by abrogating endogenous glutamate/Ca2+-mediated neurotoxicity", NEUROSCIENC, 104(3), 2001, pp. 769-781

Abstract

The neurotoxic mechanism of HIV-1 envelope glycoprotein 120 (gp120) involves glutamatergic (NMDA) receptor/Ca2+-dependent excitotoxicity. mediated inpart via glia. Pro-inflammatory cytokines also mag; have roles. We have reported that pre-exposure of brain cultures to 'physiological' ethanol concentrations (20-30 mM) protects against neuronal damage from HIV-I gp120, butnot from the direct receptor agonist, NMDA. Using lactate dehydrogenase assays and propidium iodide staining of rat organotypic hippocampal-entorhinal cortical slice cultures we determined that ethanol's suppression of gp120neurotoxicity required at least 4 days of pretreatment. The gp120-induced neurotoxicity was accompanied by interleukin-6 elevations that were not affected by the pretreatment. However. gp120 induced substantial. early increases in extracellular glutamate levels that were blocked by ethanol pretreatment. conceivably abrogating excitotoxicity. Consistent with abrogation of excitotoxic pathways. fura-2 imaging showed selective deficits in gp120-dependent intracellular Ca2+ responses in ethanol-pretreated slices. Gp120 is believed to increase glutamate levels by both stimulating release and inhibiting (re)uptake. Results with a labeled glutamate analog, D-[H-3]aspartate, revealed that gp120's inhibition of glutamate uptake, rather than its stimulation of release. was abolished after ethanol. Further studies indicatedthat two converging effects of ethanol pretreatment may underlie the abolishment of gp120-mediated glutamate uptake inhibition: (a) blockade of gp120-induced release (ostensibly from glia) of arachidonic acid, an inhibitor of astroglial glutamate reuptake, and (b) modest proliferation and activation of astroglia upon gp120 stimulation - which are likely to augment glutamate transporters. Thus. as with gp120 itself. glia and glutamate/arachidonicacid regulation appear to be important targets for ethanol. Since moderate ethanol consumption is as common among HIV-infected individuals as in the general population, this newly recognized neuroprotective (and apparently anti-excitotoxic) effect of ethanol withdrawal in vitro couldbe important but it requires further study before its significance. if any, is understood. (C) 2001 IBRO. Published by Elsevier Science Ltd. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 14:51:35