胆红素脑病NMDA受体的过度活化机制

目的：探讨Ｎ－甲基－Ｄ天冬氨酸（ＮＭＤＡ）受体水平胆红素脑病发生机制与防治措施。方法制作胆红素脑病动物模型基础上，在体脑内微透析提取兴奋性氨基酸（ＥＡＡ）神经递质，ＨＰＬＣ检测天冬氨酸（Ａｓｐ）、谷氨酸（Ｇｌｕ）、甘氨酸（Ｇｌ６），并给予模型动物ＮＭＤＡ受体拮抗剂ＧＡＰＡ干预，电镜检测脑组织超微结构，荧光检测脑组织ＡＴＰ与细胞内Ｃａ＾２＋含量。结果胆红素毒性脑组织ＡＴＰ含量显著降低，细胞外Ｇｌｙ与

NMDA Receptor Activity in Bilirubin Induced Encephalopathy

Objective Study the NMDA receptor activity in bilirubin induced encephalopathy and its molecular mechanism. Methods On the basis of bilirubin induction and NMDA receptor antagonist GAPA administration in guinea pigs. The brain extracellular EAA neurotransmitter was extracted with microdialysis and analysed with HPLC; then, brain tissue ATP was measured by fluorescence assay and intracellular Ca 2 was measured by fluorescence imaging analysis. Results ATP and EAA Neurotransmitter Gly were greatly increased in the bilirubin induced neurotoxicity brain; neural cytosolic Ca 2 in the bilirubin precipitated brain tissue was significantly more than that in the control group; NMDA receptor antagonist GAPA could significantly decrease the cytosolic Ca 2 overload. Conclusion EAA neurotransmitter Gly increased the sensitivity of the ligand Asp and Glu to the NMDA receptor, thus increased the NMDA receptor activity and cytosolic Ca 2 in the bilirubin precipitated brain tissue. NMDA receptor antagonist GAPA could prevent the cytosolic Ca 2 overload, and relieve brain edema.