The Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study

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 rat...

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Detalles Bibliográficos
Autores principales: Gdalyahu, Amos, Lazaro, Maria, Penagarikano, Olga, Golshani, Peyman, Trachtenberg, Joshua T., Gescwind, Daniel H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Public Library of Science 2015
Materias:
Research Article
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4423902/
https://www.ncbi.nlm.nih.gov/pubmed/25951243
http://dx.doi.org/10.1371/journal.pone.0125633
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author Gdalyahu, Amos
Lazaro, Maria
Penagarikano, Olga
Golshani, Peyman
Trachtenberg, Joshua T.
Gescwind, Daniel H.
author_facet Gdalyahu, Amos
Lazaro, Maria
Penagarikano, Olga
Golshani, Peyman
Trachtenberg, Joshua T.
Gescwind, Daniel H.
author_sort Gdalyahu, Amos
collection PubMed
description 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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spelling pubmed-44239022015-05-13 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. Gescwind, Daniel H. PLoS One Research Article 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. Public Library of Science 2015-05-07 /pmc/articles/PMC4423902/ /pubmed/25951243 http://dx.doi.org/10.1371/journal.pone.0125633 Text en © 2015 Gdalyahu et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
spellingShingle Research Article
Gdalyahu, Amos
Lazaro, Maria
Penagarikano, Olga
Golshani, Peyman
Trachtenberg, Joshua T.
Gescwind, Daniel H.
The Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study
title The Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study
title_full The Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study
title_fullStr The Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study
title_full_unstemmed The Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study
title_short The Autism Related Protein Contactin-Associated Protein-Like 2 (CNTNAP2) Stabilizes New Spines: An In Vivo Mouse Study
title_sort autism related protein contactin-associated protein-like 2 (cntnap2) stabilizes new spines: an in vivo mouse study
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4423902/
https://www.ncbi.nlm.nih.gov/pubmed/25951243
http://dx.doi.org/10.1371/journal.pone.0125633
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