论文部分内容阅读
兴奋性突触传递可以升高神经细胞内游离Ca2+浓度。神经细胞内异常增高的Ca2+作为第二信使,通过多途径钙信号转导,引起涉及蛋白质修饰的短时程反应和改变基因表达的长时程适应性反应。钙稳态失衡与细胞损伤、细胞凋亡等密切相关。钙超载可以破坏神经细胞质膜功能,影响神经塑性、蛋白质合成、神经-胶质细胞交互作用等,干扰神经发育和抑制线粒体功能,最终导致细胞死亡。本文综述了中枢神经系统损伤与神经元钙稳态紊乱关联效应的研究现状。
Excitatory synaptic transmission can increase the concentration of free Ca2 + in nerve cells. Ca2 +, an abnormally elevated intracellular nerve cell, serves as a second messenger and causes long-term adaptive responses that involve short-term reactions involving protein modification and altered gene expression through multi-channel calcium signaling. Calcium steady-state imbalance and cell damage, apoptosis and other closely related. Calcium overload can damage the neuronal plasma membrane function, affecting neuro-plasticity, protein synthesis, neuro-glial cell interactions, interfere with nerve development and inhibit mitochondrial function, eventually leading to cell death. This review summarizes the current status of the research on the association between central nervous system injury and neuronal calcium homeostasis.