Spontaneous seizures preferentially injure interneurons in the pilocarpine model of chronic spontaneous seizures

Spontaneous seizures preferentially injure interneurons in the pilocarpine model of chronic spontaneous seizures

Autor Mello, LEAM Google Scholar
Covolan, Luciene Autor UNIFESP Google Scholar
Instituição Universidade Federal de São Paulo (UNIFESP)
Resumo It is still a question of much debate whether single epileptic seizures can cause cell loss. Despite the clinical impression that epilepsy in generalis a progressive disorder, experimental evidence is not conclusive on this point. Recently, it has been shown that electrically-induced afterdischarges of less than 2 min may induce structural impairments in neurons. Here we evaluated whether spontaneous seizures would lead to similar impairments. Chronic spontaneous recurrent seizures were induced with pilocarpine (320 mg/kg, i.p.). Animals were sacrificed from 1 to 6 h either after single or multiple seizures. A Golgi-like sensitive silver-impregnation procedure was used to reveal injured neurons. Silver-impregnated dark neurons were never found in control animals nor in epileptic animals that had no behavioral seizures in the 8 h prior to sacrifice. After spontaneous seizures (injured) dark neurons were mostly interneurons and were present in hippocampus (CA1 stratum radiatum), amygdala, piriform cortex and other limbic structures. Animals with multiple seizures had a higher number of dark cells than animals with single seizures. Our findings suggest that even single generalized spontaneous tonic-clonic seizures can induce long-lasting morphological changes. Our results favor the idea that epilepsy is a progressive disorder where one seizure begets the next.
Assunto Golgi staining
temporal lobe epilepsy
silver staining
inhibitory neurons
hippocampal sclerosis
mesial temporal sclerosis
Idioma Inglês
Data 1996-12-01
Publicado em Epilepsy Research. Amsterdam: Elsevier B.V., v. 26, n. 1, p. 123-129, 1996.
ISSN 0920-1211 (Sherpa/Romeo, fator de impacto)
Editor Elsevier B.V.
Extensão 123-129
Fonte http://dx.doi.org/10.1016/S0920-1211(96)00048-4
Direito de acesso Acesso restrito
Tipo Artigo
Web of Science WOS:A1996VX95300015
URI http://repositorio.unifesp.br/handle/11600/25644

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