Amyloid-β oligomers suppress subunit-specific glutamate receptor increase during LTP.

ABSTRACT:

Introduction

Amyloid-β oligomers (AβOs) are assumed to impair the ability of learning and memory by suppressing the induction of synaptic plasticity, such as long-term potentiation (LTP) in the early stage of Alzheimer's disease. However, the direct molecular mechanism of how AβOs affect excitatory synaptic plasticity remains to be elucidated.

Methods

In order to study the effects of AβOs on LTP-associated changes of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid)-type glutamate receptor (AMPAR) movement, we performed live-cell imaging of fluorescently labeled AMPAR subunit GluA1 or GluA2 with total internal reflection fluorescence microscopy.

Results

Incubation of cultured hippocampal neurons with AβOs for 1-2 days inhibited the increase in GluA1 numb

SUBMITTER: Tanaka H 

PROVIDER: S-EPMC6880111 | biostudies-literature | 2019

REPOSITORIES: biostudies-literature