6-Hydroxydopamine injections into the nigrostriatal pathway attenuate striatal malonate and 3-nitropropionic acid lesions.
6-Hydroxydopamine injections into the nigrostriatal pathway attenuate striatal malonate and 3-nitropropionic acid lesions.
复制标题
6-羟基多巴胺注射到黑质纹状体通路可减轻纹状体丙二酸和 3-硝基丙酸损伤。
DOI：
10.1006/exnr.1998.6918
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发表时间：
1998
期刊：
影响因子：
--
通讯作者：
Geddes,JW
中科院分区：
文献类型：
--
作者：
Maragos,WF;Jakel,RJ;Pang,Z;Geddes,JW
The mitochondrial inhibitors malonate and 3-nitropropionic (3NP) acid are potent neurotoxinsin vivo.Administration of these compounds results in neuronal loss similar to that seen in Huntington's disease. Although the mechanism of cell death produced by these compounds likely involves activation ofN-methyl-d-aspartate receptors, it remains unclear why the striatum demonstrates regional susceptibility to the toxicity of these and other mitochondrial poisons. We hypothesized that dopamine, a weak neurotoxin that occurs in high concentrations in the striatum, may contribute to the neuronal damage caused by mitochondrial inhibition. We investigated whether depletion of striatal dopamine using the catecholaminergic toxin 6-hydroxydopamine would attenuate lesions induced by mitochondrial inhibition. We found that dopamine depletion reduced significantly the extent of histological damage in the striatum elicited by both intraparenchymal injections of 0.8 μmol malonate and 20 mg/kg systemic administration of 3NP. These data suggest that dopamine or one of its metabolites may contribute to mitochondrial toxin-induced cell death.
