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目的:研究N甲基D天冬氨酸(NMDA)诱导大鼠小脑颗粒神经元兴奋毒性保护作用的机制。方法:分别用Ca2+和Na+敏感的染料Fura2/AM和SBFI/AM测定胞内Ca2+和Na+浓度[(Ca2+)i,(Na+)i]。并用反向高效液相色谱法测定胞内三磷酸腺苷(ATP)的含量。结果:①在NMDA预处理组与非处理组,谷氨酸均迅速触发胞内Ca2+反应高峰,两者无显著性差异。而后在NMDA处理组,胞内Ca2+迅速下降,并维持在高于静息Ca2+水平的平台状,撤离谷氨酸后,[Ca2+]i迅速下降并恢复至静息水平;而NMDA非处理组则相反。②谷氨酸均诱发上述两组神经元[Na+]i升高,在NMDA非处理组,[Na+]i均高于NMDA预处理组。③谷氨酸消耗胞内ATP,而NMDA预处理组则减少胞内ATP的耗竭。结论:NMDA诱导兴奋毒性保护作用是通过减少ATP的消耗而增强胞内Ca2+和Na+的自稳态。
AIM: To investigate the protective effect of N-methyl D-aspartate (NMDA) on the excitotoxicity of cerebellar granule neurons in rats. Methods: Intracellular Ca2 + and Na + concentrations [(Ca2 +) i, (Na +) i] were determined using Fura2 / AM and SBFI / AM dyes sensitive to Ca2 + and Na +, respectively. The content of adenosine triphosphate (ATP) in the cells was determined by reverse-phase high performance liquid chromatography. Results: ① In NMDA pretreatment group and non-treatment group, glutamate rapidly triggered the peak of intracellular Ca2 + reaction, with no significant difference between the two. After NMDA treatment, intracellular Ca2 + decreased rapidly and maintained at a plateau above the level of resting Ca2 +. After withdrawal of glutamate, [Ca2 +] i decreased rapidly and returned to resting levels; whereas, NMDA non-treated . ② Glutamate induced the elevation of [Na +] i in both neurons in NMDA-treated and [Na +] i-treated groups. ③ glutamate consumes intracellular ATP, whereas NMDA preconditioning decreases intracellular ATP depletion. CONCLUSION: NMDA-induced excitotoxicity protection enhances homeostasis of intracellular Ca2 + and Na + by reducing ATP consumption.