摘要
目的 研究大鼠加速性弥漫性脑损伤后大脑皮层代谢性谷氨酸受体 1a(m Glu R1 a)的基因和蛋白表达变化与其拮抗剂 a-甲基 - 4-羧基苯氨基乙酸 (MCPG)的作用 .方法 SD大鼠 16 5只随机分为 m Glu R1 a变化和 MCPG作用 2组 .每组又分为不同的亚组 .采用 Marm arou大鼠加速性弥漫性脑损伤模型 .在伤后不同时间大鼠断头取脑进行免疫组化 ,RT- PCR技术和病理学研究 .结果 伤后 1h大脑皮层 m Glu R1 a的表达开始增加 ,2 4h达高峰 (13.9± 2 .3)· HP- 1 ,P<0 .0 1.在伤后 7d,MCPG治疗可使损伤神经元数量明显减少 (4 .2 2±1.6 3)· HP- 1 ,P<0 .0 5 .结论 m Glu R1 a参与外伤后的神经元损伤 ,其拮抗剂 MCPG可能对脑损伤有治疗作用 .
AIM To study the change of metabotropic glutamate receptor 1a (mGluR 1a ) expression in a rodent model of impact acceleration diffuse brain injury and the effect of its antagonist a-methyl-4-carboxyphenylglycine (MCPG). METHODS 165 male SD rats were randomized into two groups: Changes of mGluR 1a and effect of MCPG. Each group was redivided into different subgroups. After Marmarouou's rodent model of impact acceleration diffuse brain injury, rats were decapitated as planned and the cerebral cortex mGluR 1a was examined by immunohistochemistry,RT-PCR and the effect of MCPG was examined by pathological method at different time after injury. RESULTS At 1h after injury the expression of mGluR 1a increased and the most robust increase occurred at 24 h after injury in the injured cerebral cortex (13.9±2.3)·HP -1 , P <0.01. Administration of MCPG reduced total cortical necrotic neurons counts on the 7 day after injury (4.22±1.63)·HP -1 , P <0.05. CONCLUSION The change of mGluR 1a after traumatic brain injury and the neuroprotective effects of MCPG suggest that the activation of mGluR 1a contributes to post-traumatic neuronal damage and that MCPG may have therapeutic potential in head injury.
出处
《第四军医大学学报》
北大核心
2001年第7期612-615,共4页
Journal of the Fourth Military Medical University
基金
全军"九五"基金!资助项目 (98M10 1)
