期刊
NEURON
卷 58, 期 5, 页码 749-762出版社
CELL PRESS
DOI: 10.1016/j.neuron.2008.04.011
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资金
- MRC [MC_U122669937] Funding Source: UKRI
- Medical Research Council [MC_U122669937] Funding Source: researchfish
- Medical Research Council [MC_U122669937] Funding Source: Medline
- NIMH NIH HHS [R01 MH066676-05, R01MH66676, R01 MH066676] Funding Source: Medline
At synapses, cell adhesion molecules (CAMs) provide the molecular framework for coordinating signaling events across the synaptic cleft. Among synaptic CAMs, the integrins, receptors for extracellular matrix proteins and counterreceptors on adjacent cells, are implicated in synapse maturation and plasticity and memory formation. However, little is known about the molecular mechanisms of integrin action at central synapses. Here, we report that postsynaptic beta 3 integrins control synaptic strength by regulating AMPA receptors (AMPARs) in a subunit-specific manner. Pharmacological perturbation targeting beta 3 integrins promotes endocytosis of GluR2-containing AMPARs via Rap1 signaling, and expression of beta 3 integrins produces robust changes in the abundance and composition of synaptic AMPARs without affecting dendritic spine structure. Importantly, homeostatic synaptic scaling induced by activity deprivation elevates surface expression of beta 3 integrins, and in turn, beta 3 integrins are required for synaptic scaling. Our findings demonstrate a key role for integrins in the feedback regulation of excitatory synaptic strength.
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