Contribution of mGluR5 to hippocampal 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. Here we show using a mouse with the same genetic deficiency that metabotropic glutamate receptor 5-(mGluR5-) dependent synaptic...

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Autores principales: Tian, Di, Stoppel, Laura J., Heynen, Arnold J., Lindemann, Lothar, Jaeschke, Georg, Mills, Alea A., Bear, Mark F.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: 2015
Materias:
Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4323380/
https://www.ncbi.nlm.nih.gov/pubmed/25581360
http://dx.doi.org/10.1038/nn.3911
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author Tian, Di
Stoppel, Laura J.
Heynen, Arnold J.
Lindemann, Lothar
Jaeschke, Georg
Mills, Alea A.
Bear, Mark F.
author_facet Tian, Di
Stoppel, Laura J.
Heynen, Arnold J.
Lindemann, Lothar
Jaeschke, Georg
Mills, Alea A.
Bear, Mark F.
author_sort Tian, Di
collection PubMed
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. Here we show using a mouse with the same genetic deficiency that metabotropic glutamate receptor 5-(mGluR5-) dependent synaptic plasticity and protein synthesis is altered in the hippocampus, and that hippocampus-dependent memory is impaired. Remarkably, chronic treatment with a negative allosteric modulator of mGluR5 reverses the cognitive deficit.
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spelling pubmed-43233802015-08-01 Contribution of mGluR5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion Tian, Di Stoppel, Laura J. Heynen, Arnold J. Lindemann, Lothar Jaeschke, Georg Mills, Alea A. Bear, Mark F. Nat Neurosci Article 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. Here we show using a mouse with the same genetic deficiency that metabotropic glutamate receptor 5-(mGluR5-) dependent synaptic plasticity and protein synthesis is altered in the hippocampus, and that hippocampus-dependent memory is impaired. Remarkably, chronic treatment with a negative allosteric modulator of mGluR5 reverses the cognitive deficit. 2015-01-12 2015-02 /pmc/articles/PMC4323380/ /pubmed/25581360 http://dx.doi.org/10.1038/nn.3911 Text en http://www.nature.com/authors/editorial_policies/license.html#terms Users may view, print, copy, and download text and data-mine the content in such documents, for the purposes of academic research, subject always to the full Conditions of use:http://www.nature.com/authors/editorial_policies/license.html#terms
spellingShingle Article
Tian, Di
Stoppel, Laura J.
Heynen, Arnold J.
Lindemann, Lothar
Jaeschke, Georg
Mills, Alea A.
Bear, Mark F.
Contribution of mGluR5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
title Contribution of mGluR5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
title_full Contribution of mGluR5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
title_fullStr Contribution of mGluR5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
title_full_unstemmed Contribution of mGluR5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
title_short Contribution of mGluR5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
title_sort contribution of mglur5 to hippocampal pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4323380/
https://www.ncbi.nlm.nih.gov/pubmed/25581360
http://dx.doi.org/10.1038/nn.3911
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