Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 1 de 1
Filtrar
Mais filtros










Base de dados
Intervalo de ano de publicação
1.
Neurochem Int ; 49(7): 651-64, 2006 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-16828199

RESUMO

In the present in situ hybridization and immunocytochemical studies in the mouse central nervous system (CNS), a strong expression of spastin mRNA and protein was found in Purkinje cells and dentate nucleus in the cerebellum, in hippocampal principal cells and hilar neurons, in amygdala, substantia nigra, striatum, in the motor nuclei of the cranial nerves and in different layers of the cerebral cortex except piriform and entorhinal cortices where only neurons in layer II were strongly stained. Spastin protein and mRNA were weakly expressed in most of the thalamic nuclei. In selected human brain regions such as the cerebral cortex, cerebellum, hippocampus, amygdala, substania nigra and striatum, similar results were obtained. Electron microscopy showed spastin immunopositive staining in the cytoplasma, dendrites, axon terminals and nucleus. In the mouse pilocarpine model of status epilepticus and subsequent temporal lobe epilepsy, spastin expression disappeared in hilar neurons as early as at 2h during pilocarpine induced status epilepticus, and never recovered. At 7 days and 2 months after pilocarpine induced status epilepticus, spastin expression was down-regulated in granule cells in the dentate gyrus, but induced expression was found in reactive astrocytes. The demonstration of widespread distribution of spastin in functionally different brain regions in the present study may provide neuroanatomical basis to explain why different neurological, psychological disorders and cognitive impairment occur in patients with spastin mutation. Down-regulation or loss of spastin expression in hilar neurons may be related to their degeneration and may therefore initiate epileptogenetic events, leading to temporal lobe epilepsy.


Assuntos
Adenosina Trifosfatases/metabolismo , Encéfalo/metabolismo , Epilepsia do Lobo Temporal/metabolismo , Hipocampo/metabolismo , Estado Epiléptico/metabolismo , Adenosina Trifosfatases/genética , Animais , Astrócitos/metabolismo , Astrócitos/ultraestrutura , Encéfalo/anatomia & histologia , Convulsivantes , Giro Denteado/efeitos dos fármacos , Giro Denteado/metabolismo , Giro Denteado/fisiopatologia , Modelos Animais de Doenças , Regulação para Baixo/efeitos dos fármacos , Regulação para Baixo/fisiologia , Epilepsia/induzido quimicamente , Epilepsia/metabolismo , Epilepsia/fisiopatologia , Epilepsia do Lobo Temporal/fisiopatologia , Gliose/induzido quimicamente , Gliose/metabolismo , Gliose/fisiopatologia , Hipocampo/efeitos dos fármacos , Hipocampo/fisiopatologia , Humanos , Masculino , Camundongos , Microscopia Eletrônica de Transmissão , Agonistas Muscarínicos , Neurônios/metabolismo , Neurônios/ultraestrutura , Pilocarpina , RNA Mensageiro/metabolismo , Espastina , Especificidade da Espécie , Estado Epiléptico/fisiopatologia
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA
...