兴奋性氨基酸毒性与缺血性脑损伤  

Excitatory Amino Acid Toxicity and Ischemic Brain Injury

作　　者：赵刚[1] 李树清[1] 

机构地区：[1]昆明医学院病理生理学教研室,650031

出　　处：《国外医学（脑血管疾病分册）》2004年第6期426-429,共4页Foreign Medical Sciences Cerebrovascular Diseases

摘　　要：氨基酸作为重要的神经递质 ,对正常大脑的生理活动有调节作用。脑缺血时 ,神经元释放的谷氨酸是引起神经元死亡的重要原因。研究表明 ,除谷氨酸具有损伤效应外 ,甘氨酸 (Gly)也有协同作用 ,其释放增加能扩大脑缺血损害。γ 氨基丁酸 (GABA)能抑制兴奋性氨基酸释放或对抗氨基酸毒性。因为对神经元的作用各有侧重 ,所以综合分析它们的浓度变化和相互关系对缺血性脑损伤神经元死亡的本质将会有更进一步的认识 ,并为脑保护治疗的开辟新思路。As an important neuronal transmitter, amino acid has the effect of regulating the normal physiological activities of brain. Glumate (Glu) released from neurons during brain ischemia is a main cause of inducing neuron death. Studies have shown that in addition to the injury effect of Glu, glycine (Gly) also has the synergistic action, and its release may increase brain injury. Gamma-aminobutyric acid (GABA) can inhibit the release of excitatory Glu or resist Glu toxicity. Because they lay special emphasis on the effects of neurons respectively, synthetically analyze the change of amino acids concentration and interrelationship will further understand the essence of neuron death following brain ischemia, and find a new way in the brain protective treatment.

关 键 词：兴奋性氨基酸毒性 缺血性脑损伤 谷氨酸释放 损害机制 脑保护 

分 类 号：R743.3[医药卫生—神经病学与精神病学]