去戊烯醇增强喹啉酸对纹状体神经元的损伤

Rocío M. de Pablos, Antonio J. Herrera, Mayka Tomás-Camardiel, Alberto Machado, Josefina Cano
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引用次数: 2

摘要

我们测试了去戊烯醇对纹状体内注射喹啉酸引起的神经毒性的影响。去戊烯醇不能预防这些喹啉酸引起的损伤,但会增加γ -氨基丁酸(GABA)阳性亚群的丢失,星形胶质细胞群的丢失和喹啉酸产生的小胶质细胞的激活。这些作用是由去戊烯基增强多巴胺的作用产生的,因为先前在内侧前脑束内注射多巴胺能毒素6-羟多巴胺产生的多巴胺耗竭克服了去戊烯基的作用和多巴胺参与喹啉酸诱导的纹状体毒性。在这些条件下,喹啉酸对纹状体的毒性作用在有或没有去戊烯基处理的动物中明显较低且相似。所有这些数据都证明了为什么去丙烯醇会加重一些涉及兴奋性毒性疾病的病理信号。这也可能涉及去戊烯醇的其他副作用。
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Deprenyl enhances the striatal neuronal damage produced by quinolinic acid

We have tested the effect of deprenyl on the neurotoxicity induced by the injection of quinolinic acid within the striatum. Deprenyl was unable to prevent these quinolinic acid-induced damages, but enhanced the loss of several gamma-aminobutyric acid (GABA) positive subpopulations, the loss of the astroglial population and the activation of microglia produced by quinolinic acid. These effects are produced by deprenyl potentiation of dopamine actions since dopamine depletion produced by previous injection of the dopaminergic toxin 6-hydroxydopamine within the medial forebrain bundle overcomes deprenyl effects and the involvement of dopamine in the quinolinic acid-induced toxicity in striatum. In these conditions, quinolinic acid toxic action in striatum is significantly lower and similar in the animals treated with or without deprenyl. All these data justify why deprenyl worsen some pathological signals of disorders involving excitotoxicity. This also may be involved in other secondary effects described for deprenyl.

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