Alterations of the neocortical GABAergic system in the pilocarpine model of temporal lobe epilepsy: Neuronal damage and immunocytochemical changes in chronic epileptic rats

Alterations of the neocortical GABAergic system in the pilocarpine model of temporal lobe epilepsy: Neuronal damage and immunocytochemical changes in chronic epileptic rats

Autor Silva, A. V. Google Scholar
Sanabria, ERG Google Scholar
Cavalheiro, E. A. Google Scholar
Spreafico, R. Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Ist Nazl Neurol C Besta
Resumo A wealth of previous studies reported pathological alterations in extrahippocampal regions in mesial temporal lobe epilepsy. Previous experimental findings have also demonstrated that the entorhinal cortex and the neocortex are damaged in different animal models of acute limbic seizures. the present study was aimed at verifying possible alterations in neocortical areas, and, in particular, structural changes of GABAergic interneurons in the sensorimotor cortex, in pilocarpine-induced chronic epilepsy in the rat. Series of sections were Nissl stained and processed for immunocytochemistry using antibodies that recognize nonphosphorylated neurofilament (SMI311), glial fibrillary acidic protein (GFAP), the calcium-binding protein parvalbumin (PV) which is expressed by a subset of cortical GABAergic neurons, the GABA transporter (GAT1), and isoform 65 of glutamic acid decarboxylase (GAD65), the GABA synthetic enzyme. Epileptic rats showed decreased cortical thickness, and diffuse gliosis was observed with GFAP antibody. Neurofilament alterations were also detected in sections processed using SMI311 antiserum. in addition, a diffuse decrease of PV, GAD65, and GAT1 immunoreactivity was observed in the sensorimotor cortex. Altered expression of PV, GAD65, and GAT1 pointed out specific neocortical disturbances in GABAergic inhibition, which could play a crucial role in seizure generation and expression. Thus, the present findings indicate that damage of GABAergic interneurons could be strictly associated with neocortical hyperexcitability in temporal lobe epilepsy. (C) 2002 Elsevier Science Inc. All rights reserved.
Palavra-chave seizures
neocortex
sensorimotor cortex
parvalbumin
GABA transporter
glutamic acid decarboxylase
Idioma Inglês
Data de publicação 2002-08-15
Publicado em Brain Research Bulletin. Oxford: Pergamon-Elsevier B.V., v. 58, n. 4, p. 417-421, 2002.
ISSN 0361-9230 (Sherpa/Romeo, fator de impacto)
Publicador Elsevier B.V.
Extensão 417-421
Fonte http://dx.doi.org/10.1016/S0361-9230(02)00811-0
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:000178267000012
Endereço permanente http://repositorio.unifesp.br/handle/11600/26949

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