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β-amyloid impairs the regulation of N-methyl-D-aspartate receptors by glycogen synthase kinase 3.

Abstract：

:Accumulating evidence suggests that glycogen synthase kinase 3 (GSK-3) is a multifunctional kinase implicated in Alzheimer's disease (AD). However, the synaptic actions of GSK-3 in AD conditions are largely unknown. In this study, we examined the impact of GSK-3 on N-methyl-D-aspartate receptor (NMDAR) channels, the major mediator of synaptic plasticity. Application of GSK-3 inhibitors or knockdown of GSK-3 caused a significant reduction of NMDAR-mediated ionic and synaptic current in cortical neurons, whereas this effect of GSK-3 was impaired in cortical neurons treated with β-amyloid (Aβ) or from transgenic mice overexpressing mutant amyloid precursor protein. GSK-3 activity was elevated by Aβ, and GSK-3 inhibitors failed to decrease the surface expression of NMDA receptor NR1 (NR1) and NR1/postsynaptic density-95 (PSD-95) interaction in amyloid precursor protein mice, which was associated with the diminished GSK-3 regulation of Rab5 activity that mediates NMDAR internalization. Consequently, GSK-3 inhibitor lost the capability of protecting neurons against N-methyl-D-aspartate-induced excitotoxicity in Aβ-treated neurons. These results have provided a novel mechanism underlying the involvement of GSK-3 in AD.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Deng Y,Xiong Z,Chen P,Wei J,Chen S,Yan Z

doi

10.1016/j.neurobiolaging.2013.08.031

subject

Has Abstract

pub_date

2014-03-01 00:00:00

pages

449-59

issue

3

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(13)00382-5

journal_volume

35

pub_type

杂志文章

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