N-甲基-D-天冬氨酸型谷氨酸受体的调节与氰化物中枢毒作用

摘要/Abstract

摘要： 氰化物可通过间接与直接两条途径激活(N-甲基-D-天冬氨酸型)NMDA受体,首先氰化物引起的能量障碍能通过促使细胞外谷氨酸(Glu)浓度增高和细胞内Ca²⁺稳态失调,间接地激活NMDA受体,其次氰化物可能作为NMDA受体直接的调节剂,通过调节NMDA受体中NR₁或NR₂亚型等半胱氨酸残基的氧化还原位点,提高NMDA受体的活性,随着间接和直接NMDA受体的激活,产生一系列由NMDA受体介导的中枢毒作用,最终导致神经元细胞损伤、凋亡及死亡。由此认为NMDA受体的激活在氰化物诱导的神经损伤机制中可能起关键的作用。

关键词: N-甲基-D-天冬氨酸型受体, 神经兴奋毒性, 氰化物中枢毒作用, 谷氨酸

Abstract: Cyanide can activate the N-methyl-D-aspartate(NMDA) receptor by two approaches directly and indirectly.Firstly cyanide-induced depletion of energy is associated with the activation of NMDA receptors indirectly by increasing extracellular glutamate (Glu) and affecting cytosolic Ca^{2 +}homeostatic mechanisms.Secondly most likely as a conditioner of the NMDA receptor, cyanide enhances NMDA receptors responses by modulating redox sites of cysteine residue located in the subunit NR₁

Key words: N-methyl-D-aspartate ( NMDA) receptor, neuronal excitotoxicity, cyanide neurotoxicity, glutamate (Glu)

中图分类号:

R962

吴波拉, 朱桐君. N-甲基-D-天冬氨酸型谷氨酸受体的调节与氰化物中枢毒作用[J]. 中国临床药理学与治疗学, 2004, 9(7): 730-733.

WU Bo-La, ZHU Tong-Jun. Relation between modulation of the N-methyl-D-aspartate receptor and cyanide-induced neurotoxicity[J]. Chinese Journal of Clinical Pharmacology and Therapeutics, 2004, 9(7): 730-733.

参考文献

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