Sautière P E, Sindou P, Couratier P, Hugon J, Wattez A, Delacourte A
Unite INSERM 156-59045, Lille, France.
Neurosci Lett. 1992 Jun 22;140(2):206-10. doi: 10.1016/0304-3940(92)90104-f.
Primary neuronal cultures were treated with glutamate to induce an increase of Tau immunoreactivity similar to that observed in Alzheimer's disease. The Tau profile of neurones in culture before and after exposure to glutamate was analyzed on immunoblots with anti-Tau, anti-paired helical filaments (PHF) and antibody specific for modified Tau. Differences were observed between treated and control cultures: glutamate induced a shift of immunodetection from the lowest to the highest molecular weight Tau isoform and an acidification of Tau proteins. However, these modifications are not exactly those observed in Alzheimer's disease since we were not able to detect 'Alzheimer-type' epitopes on Tau proteins after the glutamate exposure.
原代神经元培养物用谷氨酸处理，以诱导Tau免疫反应性增加，类似于在阿尔茨海默病中观察到的情况。用抗Tau、抗成对螺旋丝（PHF）和针对修饰Tau的特异性抗体，在免疫印迹上分析暴露于谷氨酸前后培养神经元的Tau谱。在处理过的培养物和对照培养物之间观察到差异：谷氨酸诱导免疫检测从最低分子量的Tau异构体向最高分子量的Tau异构体转变，以及Tau蛋白的酸化。然而，这些修饰并不完全是在阿尔茨海默病中观察到的那些，因为在谷氨酸暴露后，我们无法在Tau蛋白上检测到“阿尔茨海默病型”表位。
