嗅球摘除昆明小鼠自主活动和探究活动的改变及杏仁核和皮层5-HT的表达

Effects of olfactory bulbectomy on mouse locomotive activity and motivational behavior of KM mice and serotonergic neurons of frontal cortex and cortical amygdaloid nucleus

目的 观察嗅球摘除昆明小鼠自主活动和探究活动的改变，及皮质杏仁核和前额叶皮层5-羟色胺（5-HT）的表达，了解嗅球与学习和动机等高级生理活动的关系及可能机制，分析嗅球摘除昆明小鼠模拟阿尔茨海默病（AD）特征行为的可行性。方法制备嗅球摘除昆明小鼠模型，采用小鼠自主活动实验和小鼠洞板实验观察其学习记忆活动和动机活动；应用免疫组织化学方法观察皮层、皮质杏仁核5-HT的表达。结果嗅球摘除昆明小鼠术后14d出现探究活动较对照组减少[分别为（7．22±3．60）次，（24．71±14．11）次，P〈0．01]，自主活动较对照组增加[分别为（182．15±42．91）次，（122．53±19．65）次，P〈0．01]；嗅球摘除14d小鼠皮质杏仁核5-HT的表达较假手术组明显增强，图像分析皮质杏仁核5-HT阳性神经元平均光密度值增加[分别为（0．149±0．025），（0．107±0．013），P〈0．01）]；前额叶皮质的5-HT较假手术组小鼠减少，5-HT阳性神经元平均光密度值减少[分别为（0．068±0．060），（0．126±0．017），P〈0．01）]。结论嗅球摘除昆明小鼠探究活动减弱，自主活动增加，可能与皮质杏仁核5-HT能神经元增加、前额叶皮质的5-HT能神经元减少有关，与老年性痴呆患者的精神改变及生化机制相似。

Objective To explore the relation between olfactory bulb and motive,the potentiality that olfactory bulbectomy mouse mimics distinctive behaviour of Alzheimer＇ s disease, olfactory bulbectomy （OB） mouse was established,and studied on the mouse locomotive activity test, mouse pole board test,and 5-HT of cortex and cortical amygdaloid nucleus. Methods OB mouse model was established and the mice were detected the follow behavioral tests post operation： mouse locomotive activity test, mouse pole board test. After operation 14 days, each mouse was sacrificed and the brains were removed. The slices of frontal cortex, limbic system were detected the expression of 5-HT by immunohistochemistry. Results OB mice showed increased locomotive activity（7.22±3.60,24.71 ± 14.11, P 〈 0.01 ） and decreased number of exploratory behavior（ 182.15 ± 42.91,122.53 ±19.65, P 〈 0.01 ）. Inununohistochemistry showed that the staining and the number of positive cells for 5-HT of OB mice in cortex decreased（0. 068 ± 0.060,0. 126 ± 0.017, P 〈 0.01 ）, while 5-HT immunoreactive cells in cortical amygdaloid nucleus increased （0. 149 ± 0.025,0. 107 ±0. 013, P 〈 0.01 ）. Conclusion The OB mice showed impairment in motivational behavior and increased locomotive activity, which are due to increased serotonergic neuron in cortical amygdaloid nucleus and decreased serotonergic neurons in frontal cortex, which proves it may mimic the characteristic behaviour of Alzheimer disease.