Miller J J, Baimbridge K G
Brain Res. 1983 Nov 14;278(1-2):322-6. doi: 10.1016/0006-8993(83)90264-0.
The levels and distribution of calcium binding protein (CaBP) were examined in the central nervous system of rats exhibiting kindling-induced epilepsy. Following commissural kindling, the concentration of CaBP in the hippocampal formation was significantly reduced but no change was observed in levels of total soluble protein or calmodulin, another calcium-related protein. Histochemical examination of kindled animals revealed a localized depletion of CaBP-like immunoreactivity restricted to the dentate granule cell-mossy fiber system of the hippocampal formation. These data demonstrate a correlation between the loss of CaBP from dentate granule cells and kindling-induced epilepsy, the underlying mechanism of which may involve an impairment of granule cells to regulate their intracellular calcium environment when challenged with high frequency electrical stimulation.
在表现出点燃诱导癫痫的大鼠中枢神经系统中，检测了钙结合蛋白（CaBP）的水平和分布。在联合点燃后，海马结构中CaBP的浓度显著降低，但总可溶性蛋白或钙调蛋白（另一种与钙相关的蛋白）水平未观察到变化。对点燃动物的组织化学检查显示，CaBP样免疫反应性的局部缺失仅限于海马结构的齿状颗粒细胞 - 苔藓纤维系统。这些数据表明齿状颗粒细胞中CaBP的丧失与点燃诱导的癫痫之间存在相关性，其潜在机制可能涉及颗粒细胞在受到高频电刺激时调节其细胞内钙环境的能力受损。
