Administration of Levetiracetam after prolonged status epilepticus does not protect from mitochondrial dysfunction in a rodent model

被引：15

作者：

Gibbs, J. E. ^{[1
]}

Cock, H. R. ^{[1
]}

机构：

[1] Univ London St Georges Hosp, Epilepsy Grp, Ctr Clin Neurosci, London SW17 0RE, England

来源：

EPILEPSY RESEARCH | 2007年 / 73卷 / 02期

基金：

英国惠康基金;

关键词：

status epilepticus; levetiracetam; perforant pathway stimulation; mitochondrial dysfunction; glutathione;

D O I：

10.1016/j.eplepsyres.2006.09.005

中图分类号：

R74 [神经病学与精神病学];

学科分类号：

摘要：

Neuronal death and dysfunction occur after status epilepticus (SE), and is associated with mitochondrial enzyme damage. We previously showed, using the rat perforant pathway stimulation model, that levetiracetam administration (LEV; 1000 mg/kg intraperitoneal) during established SE reduces seizure severity and prevents mitochondrial dysfunction. We now show that administration of the same dose of LEV after 5 h SE, does not protect from mitochondrial dysfunction. (c) 2006 Elsevier B.V. All rights reserved.

引用

页码：208 / 212

页数：5

共 10 条

[1]

Cock HR, 2004, FOCUS ON EPILEPSY RESEARCH, P105

[2] Mitochondrial dysfunction associated with neuronal death following status epilepticus in rat [J].

Cock, HR ;

Tong, X ;

Hargreaves, IP ;

Heales, SJR ;

Clark, JB ;

Patsalos, PN ;

Thom, M ;

Groves, M ;

Schapira, AHV ;

Shorvon, SD ;

Walker, MC .

EPILEPSY RESEARCH, 2002, 48 (03) :157-168

[3] Levetiracetam: Antiepileptic properties and protective effects on mitochondrial dysfunction in experimental status epilepticus [J].

Gibbs, JE ;

Walker, MC ;

Cock, HR .

EPILEPSIA, 2006, 47 (03) :469-478

[4] Neuronal cell death in a rat model for mesial temporal lobe epilepsy is induced by the initial status epilepticus and not by later repeated spontaneous seizures [J].

Gorter, JA ;

Pereira, PMG ;

van Vliet, EA ;

Aronica, E ;

da Silva, FHL ;

Lucassen, PJ .

EPILEPSIA, 2003, 44 (05) :647-658

[5] The role of mitochondria in epileptogenesis [J].

Kunz, WS .

CURRENT OPINION IN NEUROLOGY, 2002, 15 (02) :179-184

[6] Progression of brain damage after status epilepticus and its association with epileptogenesis:: A quantitative MRI study in a rat model of temporal lobe epilepsy [J].

Nairismägi, J ;

Gröhn, OHJ ;

Kettunen, MI ;

Nissinen, J ;

Kauppinen, RA ;

Pitkänen, A .

EPILEPSIA, 2004, 45 (09) :1024-1034

[7] Administration of diazepam during status epilepticus reduces development and severity of epilepsy in rat [J].

Pitkänen, A ;

Kharatishvili, I ;

Narkilahti, S ;

Lukasiuk, K ;

Nissinen, J .

EPILEPSY RESEARCH, 2005, 63 (01) :27-42

[8] MODIFICATION OF SEIZURE ACTIVITY BY ELECTRICAL STIMULATION .2. MOTOR SEIZURE [J].

RACINE, RJ .

ELECTROENCEPHALOGRAPHY AND CLINICAL NEUROPHYSIOLOGY, 1972, 32 (03) :281-&

[9] Depletion of reduced glutathione precedes inactivation of mitochondrial enzymes following limbic status epilepticus in the rat hippocampus [J].

Sleven, H ;

Gibbs, JE ;

Heales, S ;

Thom, M ;

Cock, HR .

NEUROCHEMISTRY INTERNATIONAL, 2006, 48 (02) :75-82

[10] Neuroprotective activity of CHF3381, a putative N-methyl-D-aspartate receptor antagonist [J].

Zucchini, S ;

Buzzi, A ;

Bergamaschi, M ;

Pietra, C ;

Villetti, G ;

Simonato, M .

NEUROREPORT, 2002, 13 (16) :2071-2074

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