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Effects of NMDA Receptors in Synapses and Extrasynapses of Rat Hippocampal Neurons on Amyloid-Beta-Induced Alterations in PSD-95 Expression

Authors
  • Liu, Jinping
  • Wu, Yan
  • Chang, Lirong
  • Peng, Jing
  • Song, Yizhi
  • Lu, Tao
  • Gao, Xiulai
Type
Published Article
Journal
Neuroembryology and Aging
Publisher
S. Karger AG
Publication Date
Dec 10, 2008
Volume
5
Issue
3
Pages
116–120
Identifiers
DOI: 10.1159/000183034
Source
Karger
Keywords
License
Green
External links

Abstract

The objective of this study was to investigate the mechanism of the soluble Aβ oligomer-induced alteration in synaptic proteins. Therefore, an immunofluorescence technique was applied to investigate the changes in the expression of postsynaptic density-95 (PSD-95) protein in primary hippocampal neurons, which was exposed to Aβ25–35 after N-methyl-D-aspartate receptor (NMDAR) antagonist or agonist treatment. Results showed that Aβ25–35 downregulated PSD-95 protein in a dose- and time-dependent manner. Treatment of cells with MK-801 (a general NMDA receptor antagonist) prevented Aβ-induced PSD-95 degradation. Moreover, when extrasynaptic NMDA receptors were blocked by ifenprodil (a specific antagonist of the NR2B subunit), the Aβ-induced downregulation of PSD-95 was significantly attenuated. However, when synaptic NMDA receptors were blocked by bicuculline (a GABA receptor antagonist) in combination with MK-801, the PSD-95 degradation did not change significantly. The results suggest that Aβ-induced downregulation of PSD-95 depends on NMDAR activity, and extrasynaptic NMDA receptors may be involved in Aβ-induced synaptic protein degradation.

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