Carlock L, Walker P D, Shan Y, Gutridge K
Department of Neurology, Wayne State University School of Medicine, Detroit, MI 48201, USA.
Neuroreport. 1995 May 30;6(8):1121-4. doi: 10.1097/00001756-199505300-00012.
Although Huntington disease (HD) is characterized by the selective neurodegeneration of the basal ganglia and cerebral cortex, efforts to define the disease pathology have been complicated by the widespread expression of the disease gene (IT15) throughout the body. In this study, we examined IT15 mRNA levels during the quinolinic acid (QA) excitotoxic cascade to determine whether neuronal and/or glial expression is regulated by neurodegeneration. Following an initial increase between 1 h and 6 h, IT15 mRNA levels declined in a pattern homologous to a group of neuron-specific genes. Decreased mRNA levels after 24 h demonstrated that glial transcription is not activated by neurodegeneration or gliosis. The 1 h and 24 h mRNA levels strongly suggest that IT15 transcription preferentially localizes to degenerating neurons.
尽管亨廷顿舞蹈症（HD）的特征是基底神经节和大脑皮层的选择性神经退行性变，但由于疾病基因（IT15）在全身广泛表达，确定该疾病病理的工作变得复杂。在本研究中，我们检测了喹啉酸（QA）兴奋性毒性级联反应期间的IT15 mRNA水平，以确定神经元和/或胶质细胞的表达是否受神经退行性变调节。在最初1小时至6小时之间增加之后，IT15 mRNA水平以与一组神经元特异性基因同源的模式下降。24小时后mRNA水平降低表明神经退行性变或胶质增生未激活胶质细胞转录。1小时和24小时的mRNA水平强烈表明IT15转录优先定位于正在退化的神经元。
