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Titolo:
Vigabatrin protects against hippocampal damage but is not antiepileptogenic in the lithium-pilocarpine model of temporal lobe epilepsy
Autore:
Andre, V; Ferrandon, A; Marescaux, C; Nehlig, A;
Indirizzi:
Univ Louis Pasteur Strasbourg 1, Fac Med, INSERM U398, F-67085 Strasbourg,France Univ Louis Pasteur Strasbourg 1 Strasbourg France F-67085 asbourg,France
Titolo Testata:
EPILEPSY RESEARCH
fascicolo: 1-2, volume: 47, anno: 2001,
pagine: 99 - 117
SICI:
0920-1211(200111)47:1-2<99:VPAHDB>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
GAMMA-AMINOBUTYRIC-ACID; SPONTANEOUS RECURRENT SEIZURES; INDUCED NEURONAL DAMAGE; INTRAHIPPOCAMPAL KAINATE MODEL; INDUCED STATUS EPILEPTICUS; VISUAL-FIELD CONSTRICTION; MEDIAL ENTORHINAL CORTEX; DENTATE GRANULE CELLS; IN-SITU HYBRIDIZATION; VINYL-GABA;
Keywords:
temporal lobe epilepsy; neuronal damage; GAD67; interneurons;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
89
Recensione:
Indirizzi per estratti:
Indirizzo: Nehlig, A Univ Louis Pasteur Strasbourg 1, Fac Med, INSERM U398, 11 Rue Humann, F-67085 Strasbourg, France Univ Louis Pasteur Strasbourg 1 11 Rue Humann Strasbourg France F-67085
Citazione:
V. Andre et al., "Vigabatrin protects against hippocampal damage but is not antiepileptogenic in the lithium-pilocarpine model of temporal lobe epilepsy", EPILEPSY R, 47(1-2), 2001, pp. 99-117

Abstract

In temporal lobe epilepsy (TLE), the nature of the structures involved in the development of the epileptogenic circuit is still not clearly identified. In the lithium-pilocarpine model, neuronal damage occurs both in the structures belonging to the circuit of initiation and maintenance of the seizures (forebrain limbic system) as well as in the propagation areas (cortex and thalamus) and in the circuit of remote control of seizures (substantia nigra pars reticulata). In order to determine whether protection of some brain areas could prevent the epileptogenesis induced by status epilepticus (SE) and to identify the cerebral structures involved in the genesis of TLE, we studied the effects of the chronic exposure to Vigabatrin (gamma-vinyl-GABA, GVG) on neuronal damage and epileptogenesis induced by lithium-pilocarpine SE. The animals were subjected to SE and GVG treatment (250 mg/kg) wasinitiated at 10 min after pilocarpine injection and maintained daily for 45 days. These pilo-GVG rats were compared with rats subjected to SE followed by a daily saline treatment (pilo-saline) and to control rats not subjected to SE (saline-saline). GVG treatment induced a marked. almost total neuroprotection in CA3. an efficient protection in CA1 and a moderate one in the hilus of the dentate gyrus while damage in the entorhinal cortex was slightly worsened by the treatment. All pilo-GVG and pilo-saline rats became epileptic after the same latency. Glutamic acid decarboxylase (GAD67) immunoreactivity was restored in pilo-GVG rats compared with pilo-saline rats in all areas of the hippocampus, while it was increased over control levels in the optical layer of the superior colliculus and the substantia nigra pars reticulata. Thus, the present data indicate that neuroprotection of principal cells in the Ammon's horn of the hippocampus is not sufficient to prevent epileptogenesis, suggesting that the hilus and extra-hippocampal structures, that were not protected in this study, may play a role in the genesis of spontaneous recurrent seizures in this model. Further-more. the study performed in non-epileptic rats indicates that chronic treatment with a GABAmimetic drug upregulates the expression of the protein GAD67 in specific areas of the brain. independently from the seizures. (C) 2001 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 17/02/20 alle ore 17:18:07