Contribution of mGluR5 to pathophysiology in a mouse model of human chromosome 16p11.2 microdeletion.
Nat Neurosci
; 18(2): 182-4, 2015 Feb.
Article
en En
| MEDLINE
| ID: mdl-25581360
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.
Texto completo:
1
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Piridinas
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Trastorno Autístico
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Trastornos de los Cromosomas
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Receptor del Glutamato Metabotropico 5
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Hipocampo
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Imidazoles
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Trastornos de la Memoria
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Discapacidad Intelectual
Límite:
Animals
Idioma:
En
Revista:
Nat Neurosci
Asunto de la revista:
NEUROLOGIA
Año:
2015
Tipo del documento:
Article