Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion

Microdeletions of chromosome 16p11.2 can cause autism, but the pathogenic mechanisms remain unclear. Here the authors show that in a 16p11.2 mouse model, mGluR5 synaptic plasticity and protein synthesis are altered and that a modulator of mGluR5 reverses the cognitive deficits.