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Titolo:
IMPROVEMENT OF ISCHEMIC DAMAGE IN GERBIL HIPPOCAMPAL-NEURONS BY PROCAINE
Autore:
CHEN JF; ADACHI N; LIU KY; NAGARO T; ARAI T;
Indirizzi:
EHIME UNIV,SCH MED,DEPT ANESTHESIOL & RESUSCITOL SHIGENOBU EHIME 7910295 JAPAN EHIME UNIV,SCH MED,DEPT ANESTHESIOL & RESUSCITOL SHIGENOBU EHIME 7910295 JAPAN
Titolo Testata:
Brain research
fascicolo: 1, volume: 792, anno: 1998,
pagine: 16 - 23
SICI:
0006-8993(1998)792:1<16:IOIDIG>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBRAL-ISCHEMIA; RYANODINE RECEPTOR; INTRACELLULAR CA2+; LOCAL-ANESTHETICS; RAT HIPPOCAMPUS; GLUTAMATE; SLICES; BRAIN; MECHANISMS; TRANSIENT;
Keywords:
ANOXIC DEPOLARIZATION; CA2+; CEREBRAL ISCHEMIA; GERBIL; HIPPOCAMPUS; PROCAINE;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
29
Recensione:
Indirizzi per estratti:
Citazione:
J.F. Chen et al., "IMPROVEMENT OF ISCHEMIC DAMAGE IN GERBIL HIPPOCAMPAL-NEURONS BY PROCAINE", Brain research, 792(1), 1998, pp. 16-23

Abstract

Acute cerebral ischemia induces membrane depolarization in the neuron, thereby incurring the simultaneous influx of various ions such as Na and Ca+. Since procaine possesses the ability to inhibit the releaseof Ca2+ from intracellular Ca2+ stores to the cytosol as well as the ability to block Naf channels, the effects of procaine on ischemia were investigated in the present study in gerbils both in vivo and in vitro. The histologic outcome was evaluated 7 days after 3 min of transient forebrain ischemia by assessing delayed neuronal death in hippocampal CA1 pyramidal cells in animals administered procaine (0.2, 0.4, or 2 mu mol) intracerebroventricularly 10 min before ischemia and in animals given saline. The changes in the direct-current potential shift inthe hippocampal CA1 area were measured using an identical animal model. A hypoxia-induced intracellular Ca2+ increase was evaluated by in vitro microfluorometry in gerbil hippocampal slices, and the effects ofprocaine (10, 50, and 100 mu mol/l) on the Ca2+ accumulation were examined. Additionally, the effect of procaine (100 mu mol/l) in a Ca2+-free condition was investigated. The histologic outcome was improved and the onset of the ischemia-induced membrane depolarization was prolonged by the preischemic administration of procaine. The increase in theintracellular concentration of Ca2+ induced by the in vitro hypoxia was suppressed by the perfusion of procaine-containing mediums (50 and 100 mu mol/l), regarding both the initiation and the extent of the increase. A hypoxia-induced intracellular Ca2+ elevation in the Ca2+-freecondition was observed, and the perfusion with procaine (100 mu mol/l) inhibited this elevation. Procaine helps protect neurons from ischemia by suppressing the direct-current potential shift and by inhibitingthe release of Ca2+ from the intracellular Ca2+ stores, as well as byinhibiting the influx of Ca2+ from the extracellular space. (C) 1998 Elsevier Science B.V.

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Documento generato il 02/04/20 alle ore 17:45:40