脑震荡鼠水迷宫空间认知障碍与脑胆碱能神经元变化的关系

目的探讨脑震荡（BC）鼠认知障碍与大脑胆碱能神经元变化的关系。方法成年SD大鼠84只，用自制单摆式机械打击装置，复制脑震荡大鼠模型，随机分为脑震荡后1，2，4，8，16，24d组及对照组，每组12只。应用Morris水迷宫（MWM）实验评价空间认知功能；用抗胆碱乙酰转移酶（ChAT）抗体免疫组化方法，标记大鼠基底前脑和脑干网状结构的胆碱能神经细胞，并对ChAT阳性表达物进行定量检测。结果与对照组比较，脑震荡后3d内大鼠找到平台的时间显著延长，而4—21d时差异无统计学意义。基底前脑ChAT阳性细胞数及ChAT蛋白表达活性在脑震荡后明显减少，第8天达低谷，随后增加，至第24天接近正常；脑干网状结构ChAT蛋白表达活性在伤后第1～2天下降，随后逐渐上升，第24天达高峰。结论脑震荡大鼠的认知障碍与基底前脑、脑干网状结构胆碱能神经元的变化可能有一定联系。

The relation between the spatial cognitive deficit in MWM and the changes of cholinergic neuron after brain concussion in rats

Objective To study the correlation between cognitive dysfunction and cholinergic neuron changes in basal forebrain(BFB)and brainstem reticular formation(BSRF)areas after brain con- cussion(BC)in rats.Methods Eighty-four Spragne-Dawley rats weighing 250-310g were used.The BC rat models were reproduced by a self-made simple pendulum impact device,then the rats were ran- domized into one control group and six experimental groups(1 day,2 day,4 day,8 day,16 day,and 24 day groups;n=12 in each group).A Morris Water Maze(MWM)test was used to assess learning and memory function of the rats.Cholinergic neurons in the BFB and BSRF were identified with choline acetyltransferase(CHAT)antibody and quantitated.Results Compared with the control group,the la- tency to find the platform in MWM was much longer on days 1-3 after BC,but there was no statistical difference on days 4-21 after BC.The cell number and the ChAT expression activity of cholinergic neu- rons in the BFB were obviously decreased after BC,and reached the lowest level at 8 days after BC,then increased gradually and nearly reached the normal level at 24 days.The ChAT expression activity in BSRF declined on the first 2 days after BC,then went up gradually,and reached the peak at the 24th day.Conclusion The spatial cognition deficit of BC rats can be detected by MWM in the early period (1-3 days after BC).There are significant changes in the number and ChAT expression activity in BFB and BSRF after BC.The change of cholinergic neurons may be correlated with cognitive deficits in BC rats.