摘要
目的 研究弥漫性脑损伤（DBI）后大鼠脑皮质代谢型谷氨酸受体（mGluRs）的变化及其意义。方法SD大鼠随机分为对照与DBI组,采用Marmarou加速性DBI模型,在伤后不同时间取样行原位杂交和病理学研究。结果 与对照组相比,DBI组脑皮质Ⅰ组mGluRs阳性神经元表达在伤后12h开始增加,24h达峰值（P<0.01）;Ⅱ组mGluRs阳性神经元表达在伤后24h开始减少,48h显著减少（P<0.01）。病理学研究提示,DBI后24h脑皮质神经元损伤严重（P<001）,与mGluRs表达变化的时间吻合。结论Ⅰ、Ⅱ组mGluRs作用不同,分别具有神经元损害和保护作用;脑损伤后,Ⅰ组mGluRs表达增加,参与DBI引起的神经元损伤,Ⅱ组mGluRs表达减少,其神经元保护作用减弱。这为阐明DBI的损伤机制及应用mGluRs激动剂和/或拮抗剂治疗提供了理论依据。
Objective To study the alteration and significance of metabotropic glutamate receptors (mGluRs) group Ⅰ, Ⅱ in cerebral cortex in diffuse brain injury(DBI). Methods The SD rats were randomized into sham and DBI groups. Based on Marmarou' s rodent model of DBI, the expression of mGluRs was observed by in situ hybridization and the pathologic study of cerebral cortex was carried out at different times after injury. The mGluRs positive neurons and damaged neurons were counted under microscope. Results Compared with that of sham group, the number of positive neurons with mGluRs in group Ⅰ increased at 12 h and peaked at 24 h (P < 0.01) while the number of positive neurons with mGluRs in group Ⅱreduced at 24 h and decreased significantly at 48 h (P < 0.01) after injury. By pathologic study the damaged neurons in cerebral cortex were accordingly increased at 24 h (P<0.01) in DBI group. Conclusion The mGluRs play different roles in DBI in which the mGluRs group I take part in the neuronal injury while mGluRs groupⅡ neuroprotection. This hypothesis suggests a theoretical foundation for the treatment of DBI with agonist or antagonist of mGluRs.
出处
《中华神经外科疾病研究杂志》
CAS
2002年第1期57-59,共3页
Chinese Journal of Neurosurgical Disease Research
基金
高等院校骨干教师资助项目
关键词
弥漫性脑损伤
谷氨酸
受体
Diffuse brain injury
Glutamates
Receptors
