在亨廷顿氏病的兴奋性毒性模型中,纹状突起神经元被神经蛋白选择性地保护。

S. Marco, E. Pérez-Navarro, E. Tolosa, E. Arenas, J. Alberch
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引用次数: 15

摘要

兴奋性毒性参与了几种神经退行性疾病的发病机制。我们利用纹状体内喹啉酸(QUIN)注射作为亨廷顿病动物模型,试图鉴定受神经turin (NRTN)保护的纹状体投射神经元的神经递质表型。在注射QUIN之前,将对照或分泌nrtn的细胞系移植到纹状体中,用逆行氟金标记和原位杂交检测纹状体投射神经元。nrtn分泌细胞系的纹状体内移植选择性地阻止了QUIN诱导的纹状体神经元的丢失及其标志物(谷氨酸脱羧酶67和前脑啡肽)mRNA水平的降低,而不影响纹状体神经元。因此,我们的研究结果表明,NRTN是纹状体神经元的一种选择性神经保护因子,这表明它可能是治疗受纹状体神经元群体影响的运动障碍的候选药物。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Striatopallidal neurons are selectively protected by neurturin in an excitotoxic model of Huntington's disease.
Excitotoxicity has been involved in the pathogenesis of several neurodegenerative disorders. Using intrastriatal quinolinic acid (QUIN) injection as an animal model of Huntington's disease, we attempt to identify the neurotransmitter phenotype of striatal projection neurons protected by neurturin (NRTN). Control or NRTN-secreting cell lines were grafted in the striatum before QUIN injection and striatal projection neurons were examined by retrograde Fluorogold labeling and in situ hybridization. Intrastriatal grafting of NRTN-secreting cell line selectively prevented the loss of striatopallidal neurons and also the decrease in the mRNA levels for their markers (glutamic acid decarboxylase 67 and preproenkephalin) induced by QUIN, without affecting striatonigral neurons. Thus, our findings show that NRTN is a selective neuroprotective factor for striatopallidal neurons, suggesting that it might be a candidate for the treatment of movement disorders in which this neuronal population is affected.
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