Meynert核毁损大鼠海马结构内胆囊收缩素阳性神经元的变化

目的观察Meynert核(NBM)毁损后大鼠海马结构内胆囊收缩素(CCK)阳性神经元的变化,初步探讨CCK参与学习记忆的机制。方法以海人酸毁损双侧NBM建立学习记忆障碍模型,用避暗回避实验进行行为学检测,免疫组织化学染色后光镜下观察并计数海马结构内的CCK阳性神经元。结果NBM受损后大鼠记忆保持力明显下降,与正常组比较具有显著性差异;NBM受损后海马结构内各区CCK阳性神经元数量明显减少,与正常组比较具有显著性差异。细胞形态的改变主要表现为胞体轮廓稍显模糊,突起变短,胞浆着色减弱。结论NBM损毁大鼠海马结构内CCK阳性神经元显著减少,其参与了NBM毁损后大鼠学习记忆的下降。

Changes of cholecystokinin-immunopositive neurons of hippocampal formation in Meynert-lesioned rats

Objective To investigate the changes of cholecystokinin(CCK)-immunopositive neurons of hippocampal formation in Meynert(NBM)-lesioned rats and to analyze preliminarily the mechanism of CCK's participating in learning and memory.Methods In this study,the memory dysfunction models were established by microinjection of kainic acid(KA) into the bilateral NBM.The passive avoidance task was used to estimate the degree of memory dysfunction.After 1-4 weeks of survival,brain sections were stained by immunohistochemical technique to show the CCK-immunopositive neurons.Then the CCK-immunopositive neurons were counted with optic microscope.Results The results indicated that lesions of NBM could remarkably disrupt memory continuance compared to that in normal group.There was a significant difference between the NBM-lesioned group and normal group in the number of CCK-positive neurons of hippocampal formation(P<0.01).There were a few changes of lesion on cell outline,for instance,the outline of cell body became slightly illegible and the processes shortened or disappeared.Conclusion The number of CCK-positive neurons in the hippocampal formation decreases significantly in NBM-destroyed rats,which shows that CCK may participate in memory dysfunction to a certain extent.