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Contribution of mGluR5 to 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.
Afiliación
  • Tian D; 1] Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. [2] The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. [3] Department of Brain and Cognitive Sciences, Massachusetts Institute o
  • Stoppel LJ; 1] Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. [2] The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. [3] Department of Brain and Cognitive Sciences, Massachusetts Institute o
  • Heynen AJ; 1] Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. [2] The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. [3] Department of Brain and Cognitive Sciences, Massachusetts Institute o
  • Lindemann L; Pharmaceuticals Division, F. Hoffmann-La Roche, Basel, Switzerland.
  • Jaeschke G; Pharmaceuticals Division, F. Hoffmann-La Roche, Basel, Switzerland.
  • Mills AA; Cold Spring Harbor Laboratory, Cold Spring Harbor, New York, USA.
  • Bear MF; 1] Howard Hughes Medical Institute, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. [2] The Picower Institute for Learning and Memory, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA. [3] Department of Brain and Cognitive Sciences, Massachusetts Institute o
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.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Piridinas / Trastorno Autístico / Trastornos de los Cromosomas / Receptor del Glutamato Metabotropico 5 / Hipocampo / Imidazoles / Trastornos de la Memoria / Discapacidad Intelectual Límite: Animals Idioma: En Revista: Nat Neurosci Asunto de la revista: NEUROLOGIA Año: 2015 Tipo del documento: Article
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Piridinas / Trastorno Autístico / Trastornos de los Cromosomas / Receptor del Glutamato Metabotropico 5 / Hipocampo / Imidazoles / Trastornos de la Memoria / Discapacidad Intelectual Límite: Animals Idioma: En Revista: Nat Neurosci Asunto de la revista: NEUROLOGIA Año: 2015 Tipo del documento: Article