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Titolo:
Post-insult activity is a major cause of delayed neuronal death in organotypic hippocampal slices exposed to glutamate
Autore:
Lahtinen, H; Autere, AM; Paalasmaa, P; Lauri, SE; Kaila, K;
Indirizzi:
Univ Helsinki, Dept Biosci, FIN-00014 Helsinki, Finland Univ Helsinki Helsinki Finland FIN-00014 ci, FIN-00014 Helsinki, Finland
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 105, anno: 2001,
pagine: 131 - 137
SICI:
0306-4522(2001)105:1<131:PAIAMC>2.0.ZU;2-U
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HIPPOCAMPUS; FOREBRAIN ISCHEMIA; CEREBRAL-ISCHEMIA; IN-VITRO; GLUCOSE DEPRIVATION; GERBIL HIPPOCAMPUS; PYRAMIDAL NEURONS; BRAIN ISCHEMIA; CA1 NEURONS; CELL-DEATH;
Keywords:
excitotoxicity; brain slice; neuronal network activity; epilepsy; ischemia; trauma;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Lahtinen, H Univ Helsinki, Dept Biosci, FIN-00014 Helsinki, Finland Univ Helsinki Helsinki Finland FIN-00014 4 Helsinki, Finland
Citazione:
H. Lahtinen et al., "Post-insult activity is a major cause of delayed neuronal death in organotypic hippocampal slices exposed to glutamate", NEUROSCIENC, 105(1), 2001, pp. 131-137

Abstract

We investigated the pathophysiological mechanisms of glutamate-induced delayed neuronal damage in rat hippocampal slice cultures [Stoppini et al. (1991) J. Neurosci. Methods 37, 173-182] with propidium iodide as a marker of cell death. Exposure of the cultures to growth medium containing 10 mM glutamate for 30 min resulted in a slowly developing degeneration of hippocampal principal cells, starting from the medial end of the CAI region and reaching the dentate gyrus by 48 h. By 24 h, most pyramidal cells in CAI were damaged. An acute phase of degeneration preceded the delayed damage at 2-6 h,affecting cells in a spatially diffuse manner. When tetrodotoxin (0.5 muM)was present during the glutamate insult, a marked protection (mean 57%, P < 0.001) of the CAI damage was observed. Rather strikingly, when tetrodotoxin was applied immediately following or even with a delay of 30 min after the insult, a similar amount of protection was achieved. In field recordingscarried out after the insult, the glutamate-treated slices exhibited spontaneously occurring negative shifts with a duration of 1-10 s and an amplitude of up to 400 muV in the CA3 region, whereas the control slices were always quiescent. Taken together, the results suggest that post-insult neuronal network activity, rather than the direct action of exogenous glutamate, is a major cause of delayed CAI pyramidal cell death in the organotypic slices. These observations may have implications in the design of neuroprotective strategies for the treatment of brain traumas which are accompanied by delayed and/or distal neuronal damage. (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 17/01/20 alle ore 20:15:12