Inhibition of AMPA receptor trafficking at hippocampal synapses by beta-amyloid oligomers: the mitochondrial contribution.

ABSTRACT:

Background

Synaptic defects represent a major mechanism underlying altered brain functions of patients suffering Alzheimer's disease (AD) 123. An increasing body of work indicates that the oligomeric forms of beta-amyloid (Abeta) molecules exert profound inhibition on synaptic functions and can cause a significant loss of neurotransmitter receptors from the postsynaptic surface, but the underlying mechanisms remain poorly understood. In this study, we investigated a potential contribution of mitochondria to Abeta inhibition of AMPA receptor (AMPAR) trafficking.

Results

We found that a brief exposure of hippocampal neurons to Abeta oligomers not only led to marked removal of AMPARs from postsynaptic surface but also impaired rapid AMPAR insertion during chemically-induced syn

SUBMITTER: Rui Y 

PROVIDER: S-EPMC2853530 | biostudies-literature | 2010 Mar

REPOSITORIES: biostudies-literature