Li Ning, Li Yang, Li Li-Juan, Zhu Ke, Zheng Yan, Wang Xiao-Min
Department of Neurobiology; Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Capital Medical University; Beijing Institute for Brain Disorders, Beijing, China.
Key Laboratory for Neurodegenerative Disorders of the Ministry of Education, Capital Medical University; Beijing Institute for Brain Disorders; Department of Physiology, Capital Medical University, Beijing, China.
Neural Regen Res. 2019 Jun;14(6):1037-1045. doi: 10.4103/1673-5374.250625.
Mounting evidence suggests that synaptic plasticity provides the cellular biological basis of learning and memory, and plasticity deficits play a key role in dementia caused by Alzheimer's disease. However, the mechanisms by which synaptic dysfunction contributes to the pathogenesis of Alzheimer's disease remain unclear. In the present study, Alzheimer's disease transgenic mice were used to determine the relationship between decreased hippocampal synaptic plasticity and pathological changes and cognitive-behavioral deterioration, as well as possible mechanisms underlying decreased synaptic plasticity in the early stages of Alzheimer's disease-like diseases. APP/PS1 double transgenic (5XFAD; Jackson Laboratory) mice and their littermates (wild-type, controls) were used in this study. Additional 6-week-old and 10-week-old 5XFAD mice and wild-type mice were used for electrophysiological recording of hippocampal dentate gyrus. For 10-week-old 5XFAD mice and wild-type mice, the left hippocampus was used for electrophysiological recording, and the right hippocampus was used for biochemical experiments or immunohistochemical staining to observe synaptophysin levels and amyloid beta deposition levels. The results revealed that, compared with wild-type mice, 6-week-old 5XFAD mice exhibited unaltered long-term potentiation in the hippocampal dentate gyrus. Another set of 5XFAD mice began to show attenuation at the age of 10 weeks, and a large quantity of amyloid beta protein was accumulated in hippocampal cells. The location of α-amino-3-hydroxy-5-methylisoxazole-4-propionic acid receptor and N-methyl-D-aspartic acid receptor subunits in synaptosomes was decreased. These findings indicate that the delocalization of postsynaptic glutamate receptors and an associated decline in synaptic plasticity may be key mechanisms in the early onset of Alzheimer's disease. The use and care of animals were in strict accordance with the ethical standards of the Animal Ethics Committee of Capital Medical University, China on December 17, 2015 (approval No. AEEI-2015-182).
越来越多的证据表明,突触可塑性为学习和记忆提供了细胞生物学基础,而可塑性缺陷在阿尔茨海默病所致痴呆中起关键作用。然而,突触功能障碍导致阿尔茨海默病发病的机制仍不清楚。在本研究中,利用阿尔茨海默病转基因小鼠来确定海马突触可塑性降低与病理变化及认知行为恶化之间的关系,以及阿尔茨海默病样疾病早期突触可塑性降低的潜在机制。本研究使用了APP/PS1双转基因(5XFAD;杰克逊实验室)小鼠及其同窝小鼠(野生型,对照)。另外,使用6周龄和10周龄的5XFAD小鼠及野生型小鼠进行海马齿状回的电生理记录。对于10周龄的5XFAD小鼠和野生型小鼠,取左侧海马进行电生理记录,右侧海马用于生化实验或免疫组织化学染色,以观察突触素水平和β淀粉样蛋白沉积水平。结果显示,与野生型小鼠相比,6周龄的5XFAD小鼠海马齿状回的长时程增强未发生改变。另一组5XFAD小鼠在10周龄时开始出现衰减,海马细胞中积累了大量β淀粉样蛋白。突触体中α-氨基-3-羟基-5-甲基异恶唑-4-丙酸受体和N-甲基-D-天冬氨酸受体亚基的定位减少。这些发现表明,突触后谷氨酸受体的错位及相关的突触可塑性下降可能是阿尔茨海默病早期发病的关键机制。动物的使用和护理严格遵循中国首都医科大学动物伦理委员会2015年12月17日的伦理标准(批准号:AEEI-2015-182)。