兴奋性神经毒性中的钙稳态失调及其在退行性病变中的作用

Calcium homeostasis deregulation in glutamate-induced excitotoxicity and its role in neurodegenerative diseases

兴奋性氨基酸受体的过度活化会导致神经元的兴奋性死亡,该过程与细胞内钙离子([Ca2+]i)稳态失调密切相关。谷氨酸兴奋毒性参与许多急慢性神经病变的发病及病程进展,提示Ca2+信号传导阻滞剂的应用可能在疾病的早期阶段就阻断病变进程,达到有效治疗。

Excitotoxicity refers to a process of neuronal death caused by excessive or prolonged activation of receptors for the excitatory amino acids, which is related to the overload of intracellular calcium （ [ Ca^2＋ ] i ） and mitochondrial depolarization. The well accepted hypothesis that Ca^2＋ plays a central role in neurotoxicity, and it mediated excitotoxicity is deeply involved in both acute and chronic neurodegeneration suggests that inhibitors of Ca^2＋ transduction, such as NMDA antagonists, might block the pathological process at an early stage and provide more effective protections.