Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
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Bear_Contribution of mGluR5.pdf
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Author(s)
Tian, Di
Lindemann, Lothar
Jaeschke, Georg
Stoppel, Laura Jane
Heynen, Arnold J.
Mills, Alea A.
Bear, Mark
Date Issued
January 2015
Journal
Nature Neuroscience
Publisher
Nature Publishing Group
Citation
Tian, Di, Laura J Stoppel, Arnold J Heynen, Lothar Lindemann, Georg Jaeschke, Alea A Mills, and Mark F Bear. “Contribution of mGluR5 to Pathophysiology in a Mouse Model of Human Chromosome 16p11.2 Microdeletion.” Nat Neurosci 18, no. 2 (January 12, 2015): 182–184.
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Author's final manuscript
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.
MIT Department
Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences
Picower Institute for Learning and Memory
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Article is made available in accordance with the publisher's policy and may be subject to US copyright law. Please refer to the publisher's site for terms of use.
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DOI of Published Version
https://doi.org/10.1038/nn.3911
