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The Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study.
Gdalyahu, Amos; Lazaro, Maria; Penagarikano, Olga; Golshani, Peyman; Trachtenberg, Joshua T; Geschwind, Daniel H; Gescwind, Daniel H.
Afiliação
  • Gdalyahu A; Department of Neurobiology, Integrative Center for Learning and Memory, Semel Institute for Neuroscience and Behavior, Brain Research Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
  • Lazaro M; Department of Neurology, Semel Institute for Neuroscience and Behavior, Program in Neurogenetics and Neurobehavioral Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
  • Penagarikano O; Department of Neurology, Semel Institute for Neuroscience and Behavior, Program in Neurogenetics and Neurobehavioral Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
  • Golshani P; Department of Neurology, Semel Institute for Neuroscience and Behavior, Program in Neurogenetics and Neurobehavioral Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
  • Trachtenberg JT; Department of Neurobiology, Integrative Center for Learning and Memory, Semel Institute for Neuroscience and Behavior, Brain Research Institute, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
  • Gescwind DH; Department of Neurology, Semel Institute for Neuroscience and Behavior, Program in Neurogenetics and Neurobehavioral Genetics, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, CA, United States of America.
PLoS One ; 10(5): e0125633, 2015.
Article em En | MEDLINE | ID: mdl-25951243
The establishment and maintenance of neuronal circuits depends on tight regulation of synaptic contacts. We hypothesized that CNTNAP2, a protein associated with autism, would play a key role in this process. Indeed, we found that new dendritic spines in mice lacking CNTNAP2 were formed at normal rates, but failed to stabilize. Notably, rates of spine elimination were unaltered, suggesting a specific role for CNTNAP2 in stabilizing new synaptic circuitry.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Espinhas Dendríticas / Proteínas de Membrana / Proteínas do Tecido Nervoso Tipo de estudo: Risk_factors_studies Limite: Animals Idioma: En Revista: PLoS One Assunto da revista: CIENCIA / MEDICINA Ano de publicação: 2015 Tipo de documento: Article País de afiliação: Estados Unidos País de publicação: Estados Unidos
Texto completo
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Espinhas Dendríticas / Proteínas de Membrana / Proteínas do Tecido Nervoso Tipo de estudo: Risk_factors_studies Limite: Animals Idioma: En Revista: PLoS One Assunto da revista: CIENCIA / MEDICINA Ano de publicação: 2015 Tipo de documento: Article País de afiliação: Estados Unidos País de publicação: Estados Unidos