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目的 观察次声作用后第 类 m Glu Rs在大鼠 CA1 区表达改变的规律和其激动剂二羧基环丙基甘氨酸 (DCG- )的作用 ,探讨次声致脑损伤的作用机制。 方法 2 0 0只 SD大鼠随机分为次声作用组和 DCG- 干预组 ,两组再分为对照组和次声作用 1次、3次、7次及 14次组 ,每组 10只。用8Hz、130 d B的次声按规定次数 ,每次作用 2 h。用原位杂交的方法检测第 类代谢型谷氨酸受体(m Glu Rs)的变化。病理学检测分组方法同上 ,每组 10只 ,光镜下测计 DCG- 干预前后损伤神经元数目 ,对实验结果进行统计分析。 结果 次声作用 1次后第 类 m Glu Rs阳性细胞数和光密度即出现改变 (P<0 .0 5 ) ;在 3次组改变最显著 (P<0 .0 1) ;7、14次组恢复至正常水平。形态学研究证实 ,DCG- 干预能明显减轻 CA1 区神经元的损伤程度。 结论 次声作用后可导致第 类 m Glu Rs合成及活性减少 ,DCG- 能有效降低次声对脑损伤的程度 ,提示第 类 m Glu Rs在次声脑损害过程中可能起保护作用
Objective To observe the regulation of the expression of m Glu Rs in rats after infrasound and the effect of its agonist dicarboxycyclopropylglycine (DCG-) on the mechanism of infrasound induced brain injury. Methods 200 SD rats were randomly divided into two groups: infrasound group and DCG-intervention group. The two groups were divided into control group and infrasound once, three times, seven times and 14 times with 10 rats in each group. With 8Hz, 130 d B infrasound according to the required number of times, each role 2 h. The in situ hybridization method was used to detect the changes of the class of metabotropic glutamate receptors (m Glu Rs). Pathological examination grouping method as above, 10 rats in each group. The number of injured neurons before and after DCG-intervention was measured under light microscope, and the experimental results were statistically analyzed. Results After infrasound for 1 time, the number of Glu Rs-positive cells and optical density of group m were changed (P <0.05); the changes were most significant in group 3 (P <0. 01); group 7 and 14 Return to normal level Morphological studies confirmed that, DCG-intervention can significantly reduce the degree of neuronal damage CA1 area. Conclusions The infrasound can lead to the decrease of the synthesis and activity of the m Glu Rs, DCG-can effectively reduce the infrasound damage to the brain, suggesting that the m Glu Rs may play a protective role in infrasound damage