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

ABSTRACT: Human chromosome 16p11.2 microdeletion is the most common gene copy number variation in autism, but the synaptic pathophysiology caused by this mutation is largely unknown. Using a mouse with the same genetic deficiency, we found that metabotropic glutamate receptor 5 (mGluR5)-dependent synaptic plasticity and protein synthesis was altered in the hippocampus and that hippocampus-dependent memory was impaired. Notably, chronic treatment with a negative allosteric modulator of mGluR5 reversed the cognitive deficit.

SUBMITTER: Tian D 

PROVIDER: S-EPMC4323380 | biostudies-literature | 2015 Feb

REPOSITORIES: biostudies-literature