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Titolo:
Synaptic depression and neuronal loss in transiently acidic hippocampal slice cultures
Autore:
Xiang, ZM; Bergold, PJ;
Indirizzi:
Suny Downstate Med Ctr, Dept Physiol & Pharmacol, Brooklyn, NY 11203 USA Suny Downstate Med Ctr Brooklyn NY USA 11203 acol, Brooklyn, NY 11203 USA
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1, volume: 881, anno: 2000,
pagine: 77 - 87
SICI:
0006-8993(20001020)881:1<77:SDANLI>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
INTRACELLULAR PH; SPREADING DEPRESSION; PYRAMIDAL NEURONS; LACTIC-ACIDOSIS; NEURAL ACTIVITY; NERVOUS-SYSTEM; BRAIN LACTATE; IN-VITRO; RAT; ISCHEMIA;
Keywords:
intracellular pH; lactate; bicarbonate; hypothermia; slice culture;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
45
Recensione:
Indirizzi per estratti:
Indirizzo: Bergold, PJ Suny Downstate Med Ctr, Dept Physiol & Pharmacol, 450 ClarksonAve, Brooklyn, NY 11203 USA Suny Downstate Med Ctr 450 Clarkson Ave Brooklyn NY USA 11203
Citazione:
Z.M. Xiang e P.J. Bergold, "Synaptic depression and neuronal loss in transiently acidic hippocampal slice cultures", BRAIN RES, 881(1), 2000, pp. 77-87

Abstract

Acidosis is a rapid and inevitable event accompanying cerebral ischemia ortrauma. We used hippocampal slice cultures to examine an immediate effect of acidosis, synaptic depression; and a delayed effect, neuronal loss. Exposure to low bicarbonate artificial cerebral spinal fluid (aCSF), pH 6.70 for 30 min at 32 degreesC, acidified intracellular pH from 7.31+/-0.12 to 6.53+/-0.08. Accompanying intracellular acidosis was a depression of synaptic responses. Both effects rapidly reversed after treatment with normal aCSF pH 7.35. Death analysis after acidosis treatment revealed no delayed neuronal loss. Increasing the duration of the acidosis to 60 min, however, inducedirreversible synaptic depression and delayed neuronal loss. Increasing acidosis temperature to 37 degreesC acidified intracellular pH and depressed synaptic responses. Delayed neuronal loss was also observed. Acidosis using lactate aCSF, pH 6.70 for 30 min at 32 degreesC acidified intracellular pH from 7.19+/-0.13 to 6.43+/-0.07 and depressed synaptic responses. After reperfusion with lactate containing aCSF pH 7.35, intracellular pH recovered yet synaptic responses remained depressed and delayed neuronal loss was observed. This suggested that, for a 30-min treatment at 32 degreesC, lactate acidosis was neurotoxic while low bicarbonate acidosis was not. Increasing the duration or temperature of low bicarbonate acidosis induced neuronal loss. These data provide additional evidence that acidosis contributes to the neurotoxicity during stroke and trauma. (C) 2000 Elsevier Science B.V. All rights reserved.

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Documento generato il 19/01/20 alle ore 11:42:01