摘要
目的探讨次声作用后鼠脑CA1区mGluR1α和mGluR5表达改变的规律,并观察其拮抗剂MCPG的作用。方法160只SD大鼠随机分为次声作用组及MCPG治疗组。两组再分为对照组及次声作用1次、7次和14次组。用8Hz、130dB的次声按规定次数,每次作用2 h。用免疫组织化学染色和原位杂交的方法检测mGluR1α和mGluR5的表达,光镜下观察MCPG治疗后神经元形态的改变。结果与对照组相比较,次声作用1次后,mGluR1α与mGluR5的阳性细胞数和吸光(A)值即改变( P∨0.05);7次组改变最显著( P∨0.01);14次组恢复至正常水平。形态学研究证实,MCPG对CA1区神经元有明显的保护作用。结论次声作用可通过mGluR1α和mGluR5介导兴奋性神经毒作用, 其活性的改变是导致次声性脑损害的因素之一,MCPG对次声性脑损伤具有保护作用。
Aim To explore the change of mGluR1αand mGluR5 expression in brain CA1 region after infrasonic action, and the role of antagonist MCPG in rats. Methods 160 SD rats were divided randomly into infrasonic damage group and MCPG therapy group. The two groups were subdivided into control group and 1-time, 7-time and 14-time groups respectively. Rats were exposed to 8Hz, 130dB infrasound two hours each time. Expression of mGluR1αand mGluR5 were detected by immunohistochemical staining and in situ hybridization methods. The morphological changes of neurons after MCPG therapy were observed under microscopes. Results Comparing with the control group, the number and the A value of mGluR1αand mGluR5 positive cells changed after one infrasonic action(P∨0.05); and the expression of mGluR1αand mGluR5 in the 7-time group were most obvious(P∨0.01); in the 14-time group, they recovered already to normal level. Morphological study confirmed that MCPG protected neurons from infrasonic damage. Conclusion Change of mGluR1αand mGluR5 activity can mediate exciting neurotoxicity after infrasonic action, and it is one of the major factors relative to neurons injury, MCPG had an protective effect on brain damage caused by infrasound.
出处
《细胞与分子免疫学杂志》
CAS
CSCD
北大核心
2001年第4期318-320,共3页
Chinese Journal of Cellular and Molecular Immunology
基金
国家自然科学基金资助
No.39870673
高等学校骨干教师资助
No.2000-65-66