急性缺氧对脑损伤大鼠脑皮层代谢型谷氨酸受体1α表达的影响

Effects of acute hypoxia on the expression of metabotropic glutamate receptor 1α in the brain cortex of rats with brain injury

目的 观察急性中度缺氧对脑损伤大鼠脑皮层代谢型谷氨酸受体 1α (metabotropicglutam ate receptor 1α,m Glu R1α)表达的影响 ,探讨缺氧诱导二次脑损伤的致伤机理。 方法 90只雄性 SD大鼠随机分为对照组 ,损伤组 (改良 Marm arou脑损伤模型 )、缺氧 (4 0 0 0 m高度 ) 10 min组、缺氧 30 m in组、损伤后缺氧 10 min组、损伤后缺氧 30 min组等 6组 ,各组在相应处理后 4h取标本 ,行免疫组化、HE染色及电镜检测。光镜下计数每高倍视野中损伤神经元及 m Glu R1α阳性神经元的数目 ,并对实验结果进行析因设计的方差分析。 结果 10 m in和 30 min缺氧对正常鼠脑皮层的显微、超微结构及 m Glu R1α表达无明显影响 (P>0 .0 5 ) ;10 m in缺氧也未导致脑损伤大鼠脑皮层显微、超微结构及 m Glu R1α表达明显改变 (P>0 .0 5 ) ;而 30 min缺氧可诱导脑损伤大鼠脑皮层显微及超微结构明显改变 ,m Glu R1α表达明显增高 (P<0 .0 1)。 结论 30 min急性中度缺氧可加剧脑损伤大鼠脑皮层神经元损伤 ,同时诱导 m Glu R1α高表达 ,提示 m Glu

Objective To detect the effects of acute moderately hypoxia on the expression of metabotropic glutamate receptor 1α in the brain cortex of rats with brain injury and to explore the traumagenic mechanism of secondary insult of hypoxia following the brain injury. Methods Ninety male SD rats were randomly separated into 6 groups( n =15): control group, traumatic group(modified Marmarou model group), hypoxia for 10 min group, hypoxia for 30min group, hypoxia for 10 min following traumatic brain injury group and hypoxia for 30 min following traumatic brain injury group. Four hours after different treatments were performed, brain specimens of each group of rats were obtained for immunohistochemistry staining, HE staining and electron microscopy detection. Damaged neurons and positive mGluR1α neurons in each high powered field were counted. The data of different groups were treated with factorial analysis and variance analysis. Results As compared with control group, the hypoxia for 10 min or 30 min had no evident effects on the microscopic structure, ultrastructure and the number of positive mGluR1α neurons of normal rats cortex ( P >0.05);As compared with traumatic group, hypoxia for 10 min following brain injury also had no obvious effects on the microscopic structure, ultrastructure and the number of positive mGluR1α neurons in the cortex of rats ( P >0.05); while hypoxia for 30 min following brain injury induced evident changes of microscopic structure and ultrastructure of brain cortex, and the number of positive mGluR1α neurons were significantly increased ( P <0.01). Conclusion Moderate acute hypoxia for 30 min following the brain injury may exacerbate the primary neuronal damage, and increase the number of positive mGluR1α neurons, which imply that mGluR1α is involved in the traumagenic process induced by secondary hypoxia.