Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
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 pla...
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| 格式: | Article |
| 語言: | en_US |
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Nature Publishing Group
2016
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| 在線閱讀: | http://hdl.handle.net/1721.1/102336 https://orcid.org/0000-0001-6673-4988 |
| _version_ | 1826206642511806464 |
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| author | Tian, Di Lindemann, Lothar Jaeschke, Georg Stoppel, Laura Jane Heynen, Arnold J. Mills, Alea A. Bear, Mark |
| author2 | Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences |
| author_facet | Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences Tian, Di Lindemann, Lothar Jaeschke, Georg Stoppel, Laura Jane Heynen, Arnold J. Mills, Alea A. Bear, Mark |
| author_sort | Tian, Di |
| collection | MIT |
| description | 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. |
| first_indexed | 2024-09-23T13:36:19Z |
| format | Article |
| id | mit-1721.1/102336 |
| institution | Massachusetts Institute of Technology |
| language | en_US |
| last_indexed | 2024-09-23T13:36:19Z |
| publishDate | 2016 |
| publisher | Nature Publishing Group |
| record_format | dspace |
| spelling | mit-1721.1/1023362022-10-01T15:59:04Z Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion Tian, Di Lindemann, Lothar Jaeschke, Georg Stoppel, Laura Jane Heynen, Arnold J. Mills, Alea A. Bear, Mark Massachusetts Institute of Technology. Department of Brain and Cognitive Sciences Picower Institute for Learning and Memory Tian, Di Stoppel, Laura Jane Heynen, Arnold J. Bear, Mark 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. National Institute of Mental Health (U.S.) (R21MH090452) Eunice Kennedy Shriver National Institute of Child Health and Human Development (U.S.) (R01HD046943) Simons Foundation (SFARI 240559) Massachusetts Institute of Technology. Simons Center for the Social Brain Eunice Kennedy Shriver National Institute of Child Health and Human Development (U.S.) (Physician-Scientist Career Development Award 5K08HD053824) National Institute of Mental Health (U.S.) (Training Grant 5T32MH074249) 2016-04-29T17:00:04Z 2016-04-29T17:00:04Z 2015-01 2014-09 Article http://purl.org/eprint/type/JournalArticle 1097-6256 1546-1726 http://hdl.handle.net/1721.1/102336 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. https://orcid.org/0000-0001-6673-4988 en_US http://dx.doi.org/10.1038/nn.3911 Nature Neuroscience 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. application/pdf Nature Publishing Group PMC |
| spellingShingle | Tian, Di Lindemann, Lothar Jaeschke, Georg Stoppel, Laura Jane Heynen, Arnold J. Mills, Alea A. Bear, Mark Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion |
| title | Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion |
| title_full | Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion |
| title_fullStr | Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion |
| title_full_unstemmed | Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion |
| title_short | Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion |
| title_sort | contribution of mglur5 to pathophysiology in a mouse model of human chromosome 16p11 2 microdeletion |
| url | http://hdl.handle.net/1721.1/102336 https://orcid.org/0000-0001-6673-4988 |
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