Author:
Li Peng,Xu Jin,Gu Huanhuan,Peng Hua,Yin You,Zhuang Jianhua
Abstract
Abstract
Background
Memantine, a low- to moderate-affinity uncompetitive N-methyl-D-aspartate receptor antagonist, has been shown to improve cognitive functions in animal models of Alzheimer’s disease (AD). Here we treated APP/PS1 AD mice with a therapeutic dose of memantine (20 mg/kg/day) and examined its underlying mechanisms in ameliorating cognitive defects.
Methods
Using behavioral, electrophysiological, optogenetic and morphology approaches to explore how memantine delay the pathogenesis of AD.
Results
Memantine significantly improved the acquisition in Morris water maze (MWM) in APP/PS1 mice without affecting the speed of swimming. Furthermore, memantine enhanced EC to CA1 synaptic neurotransmission and promoted dendritic spine regeneration of EC neurons that projected to CA1.
Conclusions
Our study reveals the underlying mechanism of memantine in the treatment of AD mice.
Publisher
Springer Science and Business Media LLC
Subject
Cellular and Molecular Neuroscience,General Neuroscience
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