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Significance Homeostatic plasticity constrains neuronal networks, allowing the brain to maintain a dynamic equilibrium. Loss of homeostatic plasticity disrupts normal brain function and has been implicated in autism spectrum disorder. Much of homeostatic regulation centers on synapses. In particular, excitatory AMPA-type glutamate receptors (AMPARs) are moved in and out of synapses to recalibrate neuronal activity. AMPARs can be inserted at the surface to compensate for inactivity or removed to compensate for hyperactivity. We found that GRIP1, an AMPAR-binding protein implicated in autism, regulates the homeostatic shuttling of AMPARs between cytoplasmic and synaptic pools. Restoring GRIP1 regulation may therefore prove therapeutically useful in autism.

GRIP1 is required for homeostatic regulation of AMPAR trafficking