树突棘
海马体
齿状回
神经科学
莫里斯水上航行任务
突触可塑性
记忆巩固
NMDA受体
海马结构
长时程增强
记忆障碍
阿尔茨海默病
心理学
生物
化学
受体
内科学
医学
认知
生物化学
疾病
作者
Eleazar Ramírez Hernández,Claudia Sánchez-Maldonado,Aleidy Patricio-Martínez,Ilhuicamina Daniel Limón
标识
DOI:10.1016/j.neulet.2022.137030
摘要
Research on the memory impairment caused by the Amyloid-β 25-35 (Aβ25-35) peptide in animal models has provided an understanding of the causes that occurs in Alzheimer's disease. However, it is uncertain whether this cognitive impairment occurs due to disruption of information encoding and consolidation or impaired retrieval of stored memory. The aim of this study was to determine the effect of the Aβ25-35 peptide on the morphology of dendritic spines and the changes in the expression of NR2B and PSD-95 in the hippocampus associated with learning and memory deficit. Vehicle or Aβ25-35 peptide (0.1 µg/µL) was bilaterally administered into the CA1 subfield of the rat hippocampus, then tested for spatial learning and memory in the Morris Water Maze. On Day 39, the morphological changes in the CA1 of the hippocampus and dentate gyrus were examined via Golgi-Cox stain. It was observed that the Aβ25-35 peptide administered in the CA1 region of the rat hippocampus induced changes to the morphology of dendritic spines and the expression of the NR2B subunit of the NMDA receptor co-localized with both the spatial memory and PSD-95 protein in the hippocampus of learning rats. We conclude that, in soluble form, the Aβ25-35 peptide perturbs synaptic plasticity, specifically in the formation of new synapses, thus promoting the progression of memory impairment.
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