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

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.

journal_name

Nat Neurosci

journal_title

Nature neuroscience

authors

Tian D,Stoppel LJ,Heynen AJ,Lindemann L,Jaeschke G,Mills AA,Bear MF

doi

10.1038/nn.3911

subject

Has Abstract

pub_date

2015-02-01 00:00:00

pages

182-4

issue

2

eissn

1097-6256

issn

1546-1726

pii

nn.3911

journal_volume

18

pub_type

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