Hong Yeon-Mi, Jo Dong-Gyu, Lee Min-Cheol, Kim So-Young, Jung Yong-Keun
Department of Life Science, Kwangju Institute of Science and Technology, 1 Oryong-dong, Puk-gu, Kwangju 500-712, South Korea.
Neurosci Lett. 2003 Apr 3;340(1):33-6. doi: 10.1016/s0304-3940(03)00067-3.
Calsenilin is a neuronal calcium binding protein that may function in calcium signaling and cell death. Kainic acid, an analog of the excitatory amino acid L-glutamate, produced excitotoxic cell death and induced the pathophysiology of status epilepticus. The expression of calsenilin was investigated in the mouse brain after kainic acid-induced seizure and seizure-induced hippocampal neuronal cell culture system using immunostaining analysis. Calsenilin was markedly decreased not only in the damaged cortex and CA3 region of hippocampus at 24 h after kainic acid-induced seizure but also in a cell-culture model of seizure-like activity. In addition, immunoreactivity of calsenilin in the hippocampus derived from human epilepsy patient was significantly decreased compared with normal brain. These results demonstrate that the reduced expression of calsenilin may functionally be associated with the pathophysiology of status epilepticus.
钙调素是一种神经元钙结合蛋白，可能在钙信号传导和细胞死亡中发挥作用。 kainic酸是兴奋性氨基酸L-谷氨酸的类似物，可导致兴奋性毒性细胞死亡并诱发癫痫持续状态的病理生理学。 使用免疫染色分析，在kainic酸诱导的癫痫发作和癫痫发作诱导的海马神经元细胞培养系统后，在小鼠脑中研究了钙调素的表达。 钙调素不仅在kainic酸诱导的癫痫发作后24小时在受损的皮质和海马CA3区域中显着降低，而且在癫痫样活动的细胞培养模型中也显着降低。 此外，与正常脑相比，来自人类癫痫患者的海马中钙调素的免疫反应性显着降低。 这些结果表明，钙调素表达的降低可能在功能上与癫痫持续状态的病理生理学相关。
