突触素
突触可塑性
PI3K/AKT/mTOR通路
莫里斯水上航行任务
嗅球
蛋白激酶B
神经科学
Gap-43蛋白
突触后密度
嗅觉系统
信号转导
海马体
突触疲劳
医学
细胞生物学
生物
内科学
中枢神经系统
受体
免疫组织化学
作者
Yuan Wang,Ani Zheng,Huan Yang,Qiang Wang,Bo Ren,Ting Guo,Qiang Jing,Hui Cao,Yujie Gao,Lei Xu,Hui Li,Ling He,Zhibin Liu
标识
DOI:10.31083/j.jin.2021.01.224
摘要
Synaptic dysfunction and neuronal loss are related to cognitive impairment of Alzheimer’s disease. Recent evidence indicates that regulating the phosphatidylinositol 3-Kinase (PI3K)/AKT/GSK-3β pathway is a therapeutic strategy for improving synaptic plasticity in Alzheimer’s disease. Here, we investigated “olfactory three-needle” effects on synaptic function and the PI3K/AKT/GSK-3β signaling pathway in β-amyloid1-42 (Aβ1-42)-induced Alzheimer’s disease rats. A three-needle olfactory bulb insertion for 28 days alleviated Aβ1-42-induced Alzheimer’s disease rats’ cognitive impairment as assessed by performance in the Morris water maze test. Furthermore, the three-needle electrode inhibited neuro-apoptosis and neuro-inflammation. It significantly upregulated the protein expression of postsynaptic density protein 95, synaptophysin, and GAP43, indicating a protective effect on hippocampal synaptic plasticity. Additionally, the activation level of PI3K/AKT signaling and the phosphorylation inactivation of GSK-3β were significantly enhanced by the “olfactory three-needle”. Our findings suggested that the three-needle acupuncture is a potential alternative to improve synaptic plasticity and neuronal survival of Alzheimer’s disease brain in rodents.
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