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缺血性神经元的死亡传统归属为坏死,大量的缺血性和创伤性脑损伤的动物实验发现,突触前谷氨酸释放入胞浆中,是缺血或损伤导致神经元坏死的关健步骤,既往将谷氨酸介导的神经元死亡认为是坏死,近来,国内外的实验证明,脑缺血也导致神经元膜上的谷氨酸受体活性增高,Ca~(2+)大量内流,谷氨酸受体拮抗剂和抗凋亡剂具有保护作用,揭示坏死和凋亡机制共同存在,本文就谷氨酸引起细胞死亡的机制及死亡方式作一综述。
Ischemic neuronal death is routinely attributed to necrosis, a large number of ischemic and traumatic brain injury in animal experiments found that pre-synaptic glutamate release into the cytoplasm, ischemia or injury leading to neuronal necrosis In recent years, experiments at home and abroad have proved that cerebral ischemia also results in increased glutamate receptor activity on neuronal membranes, Ca ~ (2+) A large number of influx, glutamate receptor antagonist and anti-apoptotic agents have a protective effect, revealing the co-existence of necrosis and apoptosis mechanisms, this article on glutamate-induced cell death mechanism and death mode are reviewed.