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Related Experiment Video

Updated: Mar 14, 2026

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Preparation of Oligomeric β-amyloid1-42 and Induction of Synaptic Plasticity Impairment on Hippocampal Slices

Published on: July 14, 2010

Amyloid-β effects on synapses and memory require AMPA receptor subunit GluA3.

Niels R Reinders¹, Yvonne Pao², Maria C Renner¹

¹Netherlands Institute for Neuroscience, Royal Netherlands Academy of Arts and Sciences, Amsterdam, 1105BA, The Netherlands.

Proceedings of the National Academy of Sciences of the United States of America

|October 7, 2016

Summary

Amyloid-beta (Aβ) causes cognitive deficits in Alzheimer's disease by impacting AMPA receptor subunit GluA3. Removing GluA3 protects against Aβ-induced synaptic and memory impairments in mouse models.

Keywords:

AMPA Alzheimer amyloid synapse

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Published on: June 17, 2015

Area of Science:

Neuroscience
Molecular Biology
Pathology

Background:

Amyloid-beta (Aβ) oligomers are implicated in early Alzheimer's disease (AD) cognitive decline.
Aβ-induced synaptic degradation and memory impairment are observed in AD mouse models.

Purpose of the Study:

To investigate the role of AMPA receptor (AMPAR) subunit GluA3 in mediating Aβ-driven synaptic and cognitive deficits.
To determine if GluA3 is essential for Aβ toxicity in the brain.

Main Methods:

Utilized AD mouse models and hippocampal neuron cultures.
Examined synaptic depression, spine loss, and long-term potentiation in the presence and absence of GluA3.
Assessed memory function in GluA3-deficient and wild-type mice exposed to Aβ.

Main Results:

Aβ-induced synaptic depression and spine loss were prevented in neurons lacking GluA3.
Aβ oligomers blocked long-term potentiation exclusively in neurons expressing GluA3.
GluA3-deficient mice did not exhibit memory impairment despite Aβ overproduction.

Conclusions:

The GluA3 subunit of AMPARs is critical for mediating the detrimental effects of Aβ on synapses.
Targeting GluA3-containing AMPARs may offer a therapeutic strategy for Alzheimer's disease.
Synaptic and cognitive deficits in early AD are dependent on the presence of GluA3.