Pasti L, Carmignoto G, Pozzan T, Battini R, Ferrari S, Lally G, Emson P C
Department of Experimental Biomedical Sciences, University of Padova, Italy.
Neuroreport. 1999 Aug 2;10(11):2367-72. doi: 10.1097/00001756-199908020-00027.
Cellular calcium handling was examined in brain slices from transgenic antisense mice with a regional deficiency in the neuronal calcium binding protein calbindin D28k and from their non transgenic wild type litter mate controls. Depolarization of brain slices with NMDA or potassium produced a prolonged elevation of neuronal calcium signal in neurons in brain slices from calbindin D28k-deficient transgenic mice. This effect was selective and was seen only in brain areas where the antisense construct produced a significant depletion of calbindin D28k protein. In other regions where calbindin D28k protein was not modified by the construct and in all glial cells whether from wild type or transgenic mice, cellular calcium handling was normal.
在神经元钙结合蛋白钙结合蛋白D28k存在区域缺陷的转基因反义小鼠及其非转基因野生型同窝对照小鼠的脑片中，对细胞钙处理进行了检测。用N-甲基-D-天冬氨酸（NMDA）或钾使脑片去极化，可使钙结合蛋白D28k缺陷转基因小鼠脑片中神经元的神经元钙信号长时间升高。这种效应具有选择性，仅在反义构建体导致钙结合蛋白D28k蛋白显著减少的脑区中可见。在构建体未修饰钙结合蛋白D28k蛋白的其他区域，以及所有野生型或转基因小鼠的神经胶质细胞中，细胞钙处理均正常。
