Tian, DiStoppel, Laura J.Heynen, Arnold J.Lindemann, LotharJaeschke, GeorgMills, Alea A.Bear, Mark F.2015-09-012015Tian, Di, Laura J. Stoppel, Arnold J. Heynen, Lothar Lindemann, Georg Jaeschke, Alea A. Mills, and Mark F. Bear. 2015. “Contribution of mGluR5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion.” Nature neuroscience 18 (2): 182-184. doi:10.1038/nn.3911. http://dx.doi.org/10.1038/nn.3911.1097-6256http://nrs.harvard.edu/urn-3:HUL.InstRepos:21462398Human 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. Here we show using a mouse with the same genetic deficiency that metabotropic glutamate receptor 5-(mGluR5-) dependent synaptic plasticity and protein synthesis is altered in the hippocampus, and that hippocampus-dependent memory is impaired. Remarkably, chronic treatment with a negative allosteric modulator of mGluR5 reverses the cognitive deficit.en-USJournal Article2015-09-0110.1038/nn.3911