| dc.contributor.author | Tian, Di | |
| dc.contributor.author | Lindemann, Lothar | |
| dc.contributor.author | Jaeschke, Georg | |
| dc.contributor.author | Stoppel, Laura Jane | |
| dc.contributor.author | Heynen, Arnold J. | |
| dc.contributor.author | Mills, Alea A. | |
| dc.contributor.author | Bear, Mark | |
| dc.date.accessioned | 2016-04-29T17:00:04Z | |
| dc.date.available | 2016-04-29T17:00:04Z | |
| dc.date.issued | 2015-01 | |
| dc.date.submitted | 2014-09 | |
| dc.identifier.issn | 1097-6256 | |
| dc.identifier.issn | 1546-1726 | |
| dc.identifier.uri | http://hdl.handle.net/1721.1/102336 | |
| dc.description.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. | en_US |
| dc.description.sponsorship | National Institute of Mental Health (U.S.) (R21MH090452) | en_US |
| dc.description.sponsorship | Eunice Kennedy Shriver National Institute of Child Health and Human Development (U.S.) (R01HD046943) | en_US |
| dc.description.sponsorship | Simons Foundation (SFARI 240559) | en_US |
| dc.description.sponsorship | Massachusetts Institute of Technology. Simons Center for the Social Brain | en_US |
| dc.description.sponsorship | Eunice Kennedy Shriver National Institute of Child Health and Human Development (U.S.) (Physician-Scientist Career Development Award 5K08HD053824) | en_US |
| dc.description.sponsorship | National Institute of Mental Health (U.S.) (Training Grant 5T32MH074249) | en_US |
| dc.language.iso | en_US | |
| dc.publisher | Nature Publishing Group | en_US |
| dc.relation.isversionof | http://dx.doi.org/10.1038/nn.3911 | en_US |
| dc.rights | 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. | en_US |
| dc.source | PMC | en_US |
| dc.title | Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion | en_US |
| dc.type | Article | en_US |
| dc.identifier.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. | en_US |
| dc.contributor.department | Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences | en_US |
| dc.contributor.department | Picower Institute for Learning and Memory | en_US |
| dc.contributor.mitauthor | Tian, Di | en_US |
| dc.contributor.mitauthor | Stoppel, Laura Jane | en_US |
| dc.contributor.mitauthor | Heynen, Arnold J. | en_US |
| dc.contributor.mitauthor | Bear, Mark | en_US |
| dc.relation.journal | Nature Neuroscience | en_US |
| dc.eprint.version | Author's final manuscript | en_US |
| dc.type.uri | http://purl.org/eprint/type/JournalArticle | en_US |
| eprint.status | http://purl.org/eprint/status/PeerReviewed | en_US |
| dspace.orderedauthors | Tian, Di; Stoppel, Laura J; Heynen, Arnold J; Lindemann, Lothar; Jaeschke, Georg; Mills, Alea A; Bear, Mark F | en_US |
| dc.identifier.orcid | https://orcid.org/0000-0001-6673-4988 | |
| mit.license | PUBLISHER_POLICY | en_US |
