Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion

Tian, D., Stoppel, L. J., Heynen, A. J., Lindemann, L., Jaeschke, G., Mills, A. A., Bear, M. F. (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

URL: http://www.ncbi.nlm.nih.gov/pubmed/25581360
DOI: 10.1038/nn.3911

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
Depositing User: Matt Covey
Date Deposited: 16 Jan 2015 20:54
Last Modified: 28 Apr 2015 19:30
PMCID: PMC4323380
Related URLs:
URI: http://repository.cshl.edu/id/eprint/31127

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