二次脑损伤后鼠脑皮层代谢性谷氨酸受体5mRNA表达改变及α-甲基-4-羧基苯丙氨酸的治疗作用

Change of metabotropic glutamate receptor subtype 5 mRNA levels in diffuse brain injury with secondary insults and effect of antagonist MCPG

目的 研究二次脑损伤后鼠脑皮层代谢性谷氨酸受体 5 (mGluR5 )mRNA的变化及Ⅰ类mGluR5拮抗剂α -甲基 - 4-羧基苯丙氨酸 (MCPG)的作用。 方法 90只SD大鼠随机分为原位杂交组 (6 0只 )和MCPG作用组 (30只 ) ,每组又分为不同的亚组。在Marmarou大鼠加速性弥漫性脑损伤模型基础上 ,采用抽血造成低血压。在伤后不同时间进行原位杂交和病理学研究。 结果 单纯脑损伤后脑皮层mGluR5mRNA于伤后 1d开始降低 ,7d最低 (P <0 .0 5 ) ;而脑损伤合并二次脑损伤组脑皮层mGluR5mRNA水平在伤后变化更明显。Ⅰ类mGluRs拮抗剂MCPG可减少二次脑损伤后的损伤神经元的数目。 结论 脑损伤可以抑制mGluR5的表达和生成 ,其作用可能与mGluR1、mGluR 1α不同 。

Objective To study the change of metabotropic glutamate receptor 5 (mGluR5) mRNA levels in a rodent model of diffuse brain injury with secondary insults and the effect of group antagonist MCPG. Methods Ninety male SD rats were randomized into an in situ hybridization group (n=60) and a MCPG group (n=30).Each group was further divided into different subgroups. Using in situ hybridization with oligonucleotide probe selected for mGluR5, we studied the mRNA levels at different time points after injury. Results The mRNA level of mGluR5 dropped on 1st day after injury and was the lowest on 7th day after injury ( P < 0.05 ) in the injury group. All these changes were aggravated in head injury with secondary insults. Administration of MCPG could reduce total cortical necrotic neurons 7 days after injury. Conclusions Head injury may inhibit the production of mGluR5 which may have protective properties for the brain during the development of head injury.