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Titolo:
Kainate excitotoxicity in organotypic hippocampal slice cultures: evidencefor multiple apoptotic pathways
Autore:
Liu, W; Liu, RL; Chun, JT; Bi, RF; Hoe, W; Schreiber, SS; Baudry, M;
Indirizzi:
Univ So Calif, Neurosci Program, Los Angeles, CA 90089 USA Univ So Calif Los Angeles CA USA 90089 Program, Los Angeles, CA 90089 USA Univ So Calif, Keck Sch Med, Dept Neurol, Los Angeles, CA 90033 USA Univ So Calif Los Angeles CA USA 90033 Neurol, Los Angeles, CA 90033 USA Univ Calif Los Angeles, Sch Med, Dept Pharmacol, Los Angeles, CA 90095 USAUniv Calif Los Angeles Los Angeles CA USA 90095 Los Angeles, CA 90095 USA
Titolo Testata:
BRAIN RESEARCH
fascicolo: 1-2, volume: 916, anno: 2001,
pagine: 239 - 248
SICI:
0006-8993(20011019)916:1-2<239:KEIOHS>2.0.ZU;2-S
Fonte:
ISI
Lingua:
ENG
Soggetto:
NEURONAL CELL-DEATH; PERMEABILITY TRANSITION PORE; CEREBRAL-ARTERY OCCLUSION; CYTOCHROME-C RELEASE; TUMOR-SUPPRESSOR P53; RECEPTOR ACTIVATION; DNA FRAGMENTATION; UP-REGULATION; KAINIC ACID; RAT-BRAIN;
Keywords:
excitotoxicity; caspase; bax; cytochrome c; mitochondrial membrane potential and kainate;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
51
Recensione:
Indirizzi per estratti:
Indirizzo: Baudry, M Univ So Calif, Neurosci Program, HNB124, Los Angeles, CA 90089 USA Univ So Calif HNB124 Los Angeles CA USA 90089 eles, CA 90089 USA
Citazione:
W. Liu et al., "Kainate excitotoxicity in organotypic hippocampal slice cultures: evidencefor multiple apoptotic pathways", BRAIN RES, 916(1-2), 2001, pp. 239-248

Abstract

The mechanisms underlying, kainate (KA) neurotoxicity are still not well understood. We previously reported that KA-mediated neuronal damage in organotypic cultures of hippocampal slices was associated with p53 induction. Recently, both bax and caspase-3 have been demonstrated to be key components of the p53-dependent neuronal death pathway. Caspase activation has also been causally related to the release of mitochondrial cytochrome c (Cyto C) in the cytoplasm as a result of the collapse of the mitochondrial membrane potential and the opening of mitochondrial permeability transition pores (mPTP). In the present study, we observed a rapid induction of bax in hippocampal slice cultures after KA treatment. In addition, the levels of Cyto C and caspase-3 were increased in the cytosol while the level of the caspase-9 precursor was decreased. There was also a complete reduction of Rhodamine 123 fluorescence after KA treatment, an indication of Delta psi (M) dissipation. Furthermore, inhibition of mPTP opening by cyclosporin A partially prevented Cyto C release, caspase activation and neuronal death. These data suggest the involvement of bax, several caspases, as well as Cyto C release in KA-elicited neuronal death. Finally, inhibition of caspase-3 activity by z-VAD-fnik only partially protected neurons from KA toxicity, implying thatmultiple mechanisms may be involved in KA excitotoxicity. (C) 2001 Published by Elsevier Science B.V.

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Documento generato il 15/01/21 alle ore 23:29:33