Journal
NATURE NEUROSCIENCE
Volume 18, Issue 2, Pages 182-184Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nn.3911
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Funding
- National Institute of Mental Health [R21MH090452, 5T32MH074249]
- NICHD [R01HD046943]
- Simons Foundation (SFARI) [240559]
- Simons Center for the Social Brain at the Massachusetts Institute of Technology
- physician-scientist career development award from the National Institute of Child Health and Human Development [5K08HD053824]
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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.
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