| First Author | Reinders NR | Year | 2016 |
| Journal | Proc Natl Acad Sci U S A | Volume | 113 |
| Issue | 42 | Pages | E6526-E6534 |
| PubMed ID | 27708157 | Mgi Jnum | J:238628 |
| Mgi Id | MGI:5823293 | Doi | 10.1073/pnas.1614249113 |
| Citation | Reinders NR, et al. (2016) Amyloid-beta effects on synapses and memory require AMPA receptor subunit GluA3. Proc Natl Acad Sci U S A 113(42):E6526-E6534 |
| abstractText | Amyloid-beta (Abeta) is a prime suspect for causing cognitive deficits during the early phases of Alzheimer's disease (AD). Experiments in AD mouse models have shown that soluble oligomeric clusters of Abeta degrade synapses and impair memory formation. We show that all Abeta-driven effects measured in these mice depend on AMPA receptor (AMPAR) subunit GluA3. Hippocampal neurons that lack GluA3 were resistant against Abeta-mediated synaptic depression and spine loss. In addition, Abeta oligomers blocked long-term synaptic potentiation only in neurons that expressed GluA3. Furthermore, although Abeta-overproducing mice showed significant memory impairment, memories in GluA3-deficient congenics remained unaffected. These experiments indicate that the presence of GluA3-containing AMPARs is critical for Abeta-mediated synaptic and cognitive deficits. |
