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Mesencephalic dopaminergic neurons protected by GDNF from axotomy-induced degeneration in the adult brain.

机译:GDNF保护的中脑多巴胺能神经元免于在成人脑中由轴切术引起的变性。

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摘要

Glial-cell-line-derived neurotrophic factor (GDNF) promotes survival of embryonic dopaminergic neurons in culture, and its expression pattern suggests a role as a transient target-derived trophic factor for dopaminergic neurons of the substantia nigra. These neurons participate in the control of motor activity, emotional status and cognition, and they degenerate in Parkinson's disease for unknown reasons. To test whether GDNF has a trophic effect on dopaminergic neurons in the adult brain, we used a rat model in which these neurons are induced to degenerate by transecting their axons within the medial forebrain bundle. We report here that axotomy resulted in loss of half the tyrosine hydroxylase-expressing neurons in the substantia nigra. This loss was largely prevented by repeated injections of GDNF adjacent to the substantia nigra. Our findings suggest that GDNF or related molecules may be useful for the treatment of Parkinson's disease.
机译:胶质细胞系衍生的神经营养因子(GDNF)促进了培养物中胚胎多巴胺能神经元的存活,其表达模式表明它是黑质多巴胺能神经元的瞬时靶标营养因子。这些神经元参与运动活动,情绪状态和认知的控制,并且由于未知原因而在帕金森氏病中退化。为了测试GDNF是否对成年大脑中的多巴胺能神经元具有营养作用,我们使用了大鼠模型,其中这些神经元通过横切内侧前脑束内的轴突而诱导退化。我们在这里报告,轴切术导致黑质中一半酪氨酸羟化酶表达神经元的损失。通过在黑质附近重复注射GDNF可以很大程度上防止这种损失。我们的发现表明,GDNF或相关分子可用于治疗帕金森氏病。

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