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Titolo:
Changes in neuronal excitability and synaptic function in a chronic model of temporal lope epilepsy
Autore:
Bernard, C; Marsden, DP; Wheal, HV;
Indirizzi:
Univ Southampton, Sch Biol Sci, Ctr Neurosci, Southampton SO16 7PX, Hants,England Univ Southampton Southampton Hants England SO16 7PX 16 7PX, Hants,England
Titolo Testata:
NEUROSCIENCE
fascicolo: 1, volume: 103, anno: 2001,
pagine: 17 - 26
SICI:
0306-4522(2001)103:1<17:CINEAS>2.0.ZU;2-D
Fonte:
ISI
Lingua:
ENG
Soggetto:
LONG-TERM POTENTIATION; CA1 PYRAMIDAL NEURONS; ACID-LESIONED HIPPOCAMPUS; RAT HIPPOCAMPUS; KAINIC ACID; EPILEPTIFORM ACTIVITY; LOBE EPILEPSY; SIMULTANEOUS EXPRESSION; SPIKE POTENTIATION; NMDA RECEPTORS;
Keywords:
long-term potentiation; long-term depression; hippocampus; CA1; potassium channels; temporal lobe epilepsy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Wheal, HV Univ Southampton, Sch Biol Sci, Ctr Neurosci, Bassett Crescent E, Southampton SO16 7PX, Hants, England Univ Southampton Bassett Crescent E Southampton Hants England SO16 7PX
Citazione:
C. Bernard et al., "Changes in neuronal excitability and synaptic function in a chronic model of temporal lope epilepsy", NEUROSCIENC, 103(1), 2001, pp. 17-26

Abstract

Long-term potentiation and depression of glutamatergic synaptic responses are accompanied by an increased Bring probability of neurons in response toa given excitatory input. This property. named excitatory postsynaptic potential/spike potentiation. has also been described in epileptic tissue and has pro-epileptic consequences. In this study, we show that excitatory postsynaptic potential/spike potentiation can be reversed in the kainic acid lesioned rat hippocampus, a chronic model of temporal lobe epilepsy. Simultaneous in vitro extracellular recordings in stratum radiatum and stratum pyramidale were performed in the CA1 area of the kainic acid lesioned rat hippocampal slices. Fifteen minutes, application of the K+ channel blocker tetraethylammonium resulted in excitatory postsynaptic potential/spike potentiation (measured 90 min after the start of the washout period) which could be reversed by subsequent low-frequency or tetanic stimuli. Excitatory post-synaptic potential/spike potentiation and its subsequent reversal by an electrical conditioning stimulus were found to have a N-methyl-D-aspartate receptor-independent component. Tetraethylammonium treatment also resulted in excitatory post-synaptic potential/spike potentiation of pharmacologically isolated N-methyl-D-aspartate receptor-mediated responses which could be reversed by subsequent low-frequency or tetanic stimuli. We conclude that excitatory postsynaptic potential/spike potentiation can be reversed in epileptic tissue, even in the absence of synaptic plasticity. These results suggest the presence of endogenous regulatory mechanisms which are able to decrease cell excitability. (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 20/01/20 alle ore 04:47:11