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Titolo:
CELLULAR MECHANISMS UNDERLYING SPONTANEOUS INTERICTAL SPIKES IN AN ACUTE MODEL OF FOCAL CORTICAL EPILEPTOGENESIS
Autore:
DECURTIS M; RADICI C; FORTI M;
Indirizzi:
IST NAZL NEUROL,DEPT EXPT NEUROPHYSIOL,VIA CELORIA 11 I-20133 MILAN ITALY
Titolo Testata:
Neuroscience
fascicolo: 1, volume: 88, anno: 1999,
pagine: 107 - 117
SICI:
0306-4522(1999)88:1<107:CMUSIS>2.0.ZU;2-L
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT HIPPOCAMPAL SLICE; GUINEA-PIG BRAIN; INDUCED EPILEPTIFORM ACTIVITY; EXCITATORY AMINO-ACID; PIRIFORM CORTEX; BURST GENERATION; OLFACTORY CORTEX; IN-VITRO; RECEPTORS; NEURONS;
Keywords:
EPILEPTOGENESIS; INTERICTAL SPIKES; INTRACELLULAR RECORDINGS; ISOLATED BRAIN PREPARATION; PIRIFORM CORTEX;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
43
Recensione:
Indirizzi per estratti:
Citazione:
M. Decurtis et al., "CELLULAR MECHANISMS UNDERLYING SPONTANEOUS INTERICTAL SPIKES IN AN ACUTE MODEL OF FOCAL CORTICAL EPILEPTOGENESIS", Neuroscience, 88(1), 1999, pp. 107-117

Abstract

The cellular mechanisms involved in the generation of spontaneous epileptiform potentials were investigated in the pirifom cortex of the invitro isolated guinea-pig brain. A single, unilateral injection of bicuculline (150-200 nmol) in the anterior piriform cortex induced locally spontaneous interictal spikes that recurred with a period of 8.81 +/- 4.47 s and propagated caudally to the ipsi- and contralateral hemispheres. Simultaneous extra- and intracellular recordings from layer IIand III principal cells showed that the spontaneous interictal spike correlates to a burst. of action potentials followed by a large afterdepolarization. Intracellular application of the sodium conductance blocker, QX-314 (80 mM), abolished bursting activity and unmasked a high-threshold slow spike enhanced by the calcium chelator EGTA (50 mM). The slow spike was abolished by membrane hyperpolarization and by local perfusion with 2 mM cadmium. The depolarizing potential that followed the primary burst was reduced by arterial perfusion with the N-methyl-D-aspartate receptor antagonist, DL-2-amino-5-phosphonopentanoic acid (100-200 mu M). The non-iv-methyl-D-aspartate glutamate receptor antagonist, 6-cyano-7-nitroquinoxaline-2,3-dione (20 mu M), completely and reversibly blocked the spontaneous spikes. The interictal spikes were terminated by a large afterpotential blocked either by intracellular QX-314 (80 mM) or by extracellular application of phaclofen and 2-hydroxysaclofen (10 and 4 mM, respectively). The present study demonstratesthat, in an acute model of epileptogenesis, spontaneous interictal spikes are fostered by a primary burst of fast action potentials that ride on a regenerative high-threshold, possibly calcium-mediated spike, which activates a recurrent, glutamate-mediated potential responsible for the entrainment of adjacent and remote cortical regions. The bursting activity is controlled by a GABA(B) receptor-mediated inhibitory synaptic potential. (C) 1998 IBRO. Published by Elsevier Science Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/04/20 alle ore 00:32:04