摘要
目的探讨丘脑底核深部脑电刺激术(STN-DBS)对帕金森病(PD)大鼠认知功能的影响及机制。方法30只SD大鼠按随机数字表法分为3组:对照组(健康大鼠,n=10)、模型组(PD大鼠,n=10)和电刺激组(PD大鼠,高频电刺激,n=10)。Morris水迷宫检测认知功能,ELISA检测皮质、海马、纹状体处的乙酰胆碱(ACh)含量。结果与对照组相比,模型组大鼠在Morris水迷宫第4天和第5天的逃避潜伏期更长[第4天(38±14)s比(20±4)s,P=0.047;第5天(32±13)s比(16±8)S,P=0.032],探索试验中在目标象限停留时间更短[(10±6)s比(19±5)s,P=0.023],海马[(1473±233)s比(1950±344)s,P=0.039]和纹状体[(1661±271)s比(2240±290)s,P=0.007]部位的ACh表达减少,电刺激组大鼠与对照组上述指标无明显差异。结论PD模型大鼠认知功能下降,STN-DBS可促进认知功能的恢复,可能与调节海马、纹状体处的乙酰胆碱含量有关。
Objective To illustrate the effect of subthalamic nucleus deep brain stimulation (STN- DBS)on cognitionand its underlying mechanisms in a rat model of Parkinson's disease (PD). Methods Thirty healthy male Sprague-Dawley rats were randomly divided into 3 groups: control group (healthy rats, n = 10 ), model group (PD rats, n = 10 ), and stimulation group (PD rats receiving high frequency stimulation, n = 10). The cognitive functionof rats was tested through Morris water maze and acetylcholine levels in cortex, hippocampus and striatum have been examined through ELISA. Results During Morris water mazetest, spatial learning and memory of PD ratsdeteriorated compared with healthy ones, withlonger escape latency[onday4, (38±14) svs (20±4) s,P=0.047;onday5, (32±13) svs (16±8) s,P= 0. 032 ] and shorter time in the platform region [ ( 10 ±6) s vs ( 19 ± 5 ) s, P = 0. 023 ] , which could be restored by STN-DBS. Similar results demonstrated that the expression of Ach in hippocampus [ ( 1 473 + 233) s vs ( 1 950 ± 344) s,P = 0. 039 ] and striatum [ ( 1 661 ± 271 ) s vs (2 240 ±290) s, P = 0. 007 ] was significantly lower in PD rats than those in healthy rats, and STN-DBS treatment reversed this decline to insignificant. Conclusion The rat model of PD suffer from a decline in cognition, and STN-DBS contributes to cognitive recovery, possibly due to regulating Ach levels in cognition-associated regions of the brain, includinghippocampus and striatum.
出处
《中华医学杂志》
CAS
CSCD
北大核心
2017年第25期1970-1974,共5页
National Medical Journal of China
关键词
帕金森病
丘脑底核
深部脑电刺激术
乙酰胆碱
认知
Parkinson' s disease
Subthalamicnucleus
Deep brain stimulation
Acetylcholine
Cognition