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本文旨在探讨突触功能障碍大鼠模型在额叶、颞叶和海马这些与认知功能有关的脑区EEC频域特征。先用海马CA1区Aβ_(1-40)微量注射法制备突触功能障碍模型,用Morris水迷宫行为学测试系统检测其学习记忆能力；然后记录上述脑区的EEC并做频谱分析。结果显示：(1)模型组在第3、4、5、6训练时间段的平均逃避潜伏期较正常组明显延长,和第2训练时间段的相比较,正常组第5训练时间段平均逃避潜伏期明显缩短,模型组到第7训练时间段平均遮避潜伏期开始明显缩短(P＜0．05)；撤去平台后,模型组在原平台所在象限的时间百分比明显降低(P＜0．05)。(2)模型组的EEG表现为α节律慢化,功率下降,其主峰频率左移2Hz,并且额叶、颞叶和海马的δ波和θ波功率不同程度地增高。由此Aβ1-40微量注射法成功制备了突触功能障碍大鼠模型。该模型大鼠的学习记忆能力降低,其频谱特征表现为α节律慢化,功率下降或消失,慢波(δ波和θ波)活动增多,功率不同程度地增高。这些与阿尔茨海默病(Alzheimer’s disease,AD)的EEG一致,可为以后对突触功能障碍时受累皮层进行深入的可塑性和神经再生的研究提供电生理基础。
This article aims to explore the synaptic dysfunction in rat models of frontal lobe, temporal lobe and hippocampus cognitive function-related brain regions EEC frequency features. Synaptic dysfunction model was prepared by microinjection of Aβ_ (1-40) in hippocampal CA1 region. Morris water maze behavior test system was used to detect the learning and memory ability. The EEC of the brain regions was recorded and analyzed. The results showed that: (1) The average evasion latency of the model group in the third, fourth, fifth and sixth training periods was significantly longer than that of the normal group, and the mean escape latency of the fifth training period in the normal group compared with the second training period (P <0.05). After withdrawal of the platform, the time percentage of model group in the quadrant of the original platform was significantly decreased (P <0.05). (2) The EEG of the model group was slowed down by α rhythm, the power decreased, the main peak frequency shifted left by 2 Hz, and the δ wave and θ wave power of frontal lobe, temporal lobe and hippocampus increased to some extent. Thus Aβ1-40 microinjection successfully prepared synaptic dysfunction rat model. The learning and memory abilities of the model rats decreased, and their spectral features showed that the rhythms of the rhythms were moderate, the power decreased or disappeared, the activities of the slow wave (δ wave and θ wave) increased, and the power increased to some extent. These are consistent with the EEG of Alzheimer’s disease (AD) and provide an electrophysiological basis for the subsequent study of the in-depth plasticity and neural regeneration of the affected cortex during synaptic dysfunction.