Tian, D., Stoppel, L. J., Heynen, A. J., Lindemann, L., Jaeschke, G., Mills, A. A., Bear, M. F. (January 2015) Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion. Nature Neuroscience, 18. pp. 182-184. ISSN 1097-6256
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.
| Item Type: | Paper |
|---|---|
| Subjects: | bioinformatics > genomics and proteomics diseases & disorders > mental disorders > personality disorders > autism bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > chromosome bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > chromosomes, structure and function > chromosome bioinformatics > genomics and proteomics > genetics & nucleic acid processing > DNA, RNA structure, function, modification > copy number variants |
| CSHL Authors: | |
| Communities: | CSHL labs > Mills lab CSHL Cancer Center Program > Gene Regulation and Inheritance Program |
| Depositing User: | Matt Covey |
| Date: | 12 January 2015 |
| Date Deposited: | 16 Jan 2015 20:54 |
| Last Modified: | 29 Oct 2020 19:10 |
| PMCID: | PMC4323380 |
| Related URLs: | |
| URI: | https://repository.cshl.edu/id/eprint/31127 |
Actions (login required)
 |
Administrator's edit/view item |