摘要
目的 :探讨 8Hz、12 0 d B次声作用后大鼠脑皮质内代谢性谷氨酸受体 5亚型 ( m Glu R5 ) m RNA表达的变化及意义。方法 :SD大鼠 60只被随机分为对照组及次声作用 1、7、14次组和次声作用组 ,采用自制的次声压力舱用 8Hz、12 0 d B的次声按规定次数 ,每次作用 2小时。利用地高辛标记寡聚核苷酸探针原位杂交技术与计算机图像分析系统 ,在光镜与透射电镜下观察 m Glu R5分别在额、顶、颞及枕皮质 1区阳性神经元表达的改变 ,以及相应皮质的病理变化。结果 :次声作用 1次组 ,额、顶、颞、枕脑皮质内 m Glu R5 m RNA阳性神经元表达减少 ,次声作用 7次组脑皮质内 m Glu R5 m RNA阳性神经元表达数减少至谷底与对照组和次声作用 1次组比较 P均 <0 .0 1,次声作用 14次组脑皮质内 m Glu R5 m RNA阳性神经元表达数基本恢复到正常水平 ;阳性神经元在脑皮质浅层散在分布 ,m Glu R5 m RNA在胞浆和胞核内均匀地呈颗粒状表达。结论 :次声脑损伤可抑制m Glu R5的表达和生成 ,其作用可能与 m Glu R1α不同 ,参与机体对次声脑损伤的保护。
Objective:To investigate the significance of changes in metabotropic glutamate receptor subtype 5(mGluR5) mRNA in brain cortex after infrasonic damage in rats.Methods:Sixty SD rats were randomly divided into four groups:control group and 1time,7time,14time infrasonic damage groups.Rats were exposed to 8 Hz 120 dB infrasound as designed,each time for two hours.The changes in mGluR5 mRNA expression and pathology of cortex in area 1 cortex of the frontal,parietal,temporal and occipital lobe were observed under light and electronic microscope with digoxinlabeled oligonucleotide probe in situ hybridization method and computer aided image analysis.Results:The expression of mGluR5 mRNA positive neurons decreased in cortex after infrasonic damage in 1time group and was most weakest in 7time group (P<0.01).While the number of mGluR5 mRNA positive neurons in 14time group nearly reached normal range.The expression of mGluR5 mRNA presented grain shape,and uniformly exist in cytoplasm and nucleus of positive neurons which dispersed in superficial cortex.Conclusions:Under infrasonic brain injury,the decrease in expression and induction of mGluR5 in brain cortex,the effect of which is probably different from the alteration in mGluR1α,may be involved in the protection mechanism underlying host to infrasonic brain injury.
出处
《中国危重病急救医学》
CAS
CSCD
2001年第8期467-469,共3页
Chinese Critical Care Medicine
基金
国家自然科学基金资助项目 ( No.39870 673)
高等学校骨干教师资助计划项目 ( No.2 0 0 0 12 0 3)
关键词
脑损伤
次声
代谢性谷氨酸受体5亚型
infrasnic brain injury
metabotropic glutamate receptor subtype 5