期刊
NEUROSCIENCE LETTERS
卷 341, 期 2, 页码 87-90出版社
ELSEVIER IRELAND LTD
DOI: 10.1016/S0304-3940(03)00172-1
关键词
mitochondria; dopamine; astrocytes; complex I; rotenone; Parkinson's disease
Chronic rotenone exposure reproduces features of Parkinson's disease (PD) (Nat. Neurosci. 3 (2000) 1301; Exp. Neurol. 179 (2003) 9). We investigated the role of glial activation in rotenone toxicity in vivo. Male Lewis rats received 2-3 mg/kg rotenone per day for up to 4 weeks. In 50% of surviving rotenone-treated animals, there was nigrostriatal dopaminergic degeneration, marked by reduced tyrosine hydroxylase immunoreactivity). Extensive microglial activation, determined by OX-42-ir, occurred in striatum and nigra of rotenone-treated animals, and was prominent before anatomical evidence of dopaminergic lesions. Microglia enlarged and developed short, stubby processes in rotenone-treated animals. Rotenone-induced microglial activation was less pronounced in cortex. Reactive astrocytosis was minimal and limited to a thin rim around the lesion. Marked microglial activation with minimal astrocytosis is another pathological feature of PD reproduced by rotenone treatment. (C) 2003 Elsevier Science Ireland Ltd. All rights reserved.
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