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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Detalles Bibliográficos
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
Descripción
Sumario: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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