论文部分内容阅读
目的 探讨胆红素脑病动物模型制作及其脑组织中兴奋性氨基酸 (EAA)神经递质变化。方法 豚鼠腹腔内给予胆红素 2 0 0 μg/g后 8h ,电镜观察脑组织形态结构 ,在体脑内微透析提取神经突触间细胞外液 ,HPLC检测分析天冬氨酸 (Asp) ,谷氨酸 (Glu)和甘氨酸 (Gly)。结果 胆红素毒性脑组织神经元及其线粒体肿胀 ,细胞外Gly含量为2 1 .35± 4.87μM ,明显高于对照组1 4 .0 2± 1 .5 6 μM (P <0 .0 1 ) ;胆红素毒性脑组织细胞外Asp ,Glu与对照组比较差异不显著 (P >0 .0 5 )。结论 胆红素毒性脑组织细胞外甘氨酸 (Gly)含量增加 ,可提高NMDA受体对EAA神经递质Asp及Glu敏感性 ,致NMDA受体过度活化。
Objective To explore the animal model of bilirubin encephalopathy and its changes of neurotransmitter of excitatory amino acid (EAA) in brain tissue. Methods The guinea pigs were intraperitoneally administered with bilirubin 200 microg / g for 8 hours. The morphology of the brain tissue was observed by electron microscopy. Extracellular synaptosomes were extracted by intracerebral microdialysis. Asp was detected by HPLC. Glutamic acid (Glu) and Glycine (Gly). Results The bilirubin neurons and their mitochondria swelled with bilirubin toxicity. The content of extracellular Gly was 21.35 ± 4.87μM, which was significantly higher than that of the control group (14.02 ± 1.56μM, P <0.01) ). There was no significant difference of extracellular Asp, Glu in brain tissue between bilirubin and control group (P> 0.05). Conclusion The increase of extracellular glycine content in bilirubin-toxic brain tissue can increase the sensitivity of NMDA receptor to Asp and Glu, which is the neurotransmitter of EAA, and cause NMDA receptor over-activation.