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

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          Abstract

          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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          The autistic neuron: troubled translation?

          Raymond J Kelleher, Mark Bear (2008)
          Autism is a complex genetic disorder, but single-gene disorders with a high prevalence of autism offer insight into its pathogenesis. Recent evidence suggests that some molecular defects in autism may interfere with the mechanisms of synaptic protein synthesis. We propose that aberrant synaptic protein synthesis may represent one possible pathway leading to autistic phenotypes, including cognitive impairment and savant abilities.
          Article 0 comments Cited 205 times – based on 0 reviews     Review now
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            Cortical rewiring and information storage.

            D. Chklovskii, B. W. Mel, K. Svoboda (2004)
            Current thinking about long-term memory in the cortex is focused on changes in the strengths of connections between neurons. But ongoing structural plasticity in the adult brain, including synapse formation/elimination and remodelling of axons and dendrites, suggests that memory could also depend on learning-induced changes in the cortical 'wiring diagram'. Given that the cortex is sparsely connected, wiring plasticity could provide a substantial boost in storage capacity, although at a cost of more elaborate biological machinery and slower learning.
            Article 0 comments Cited 191 times – based on 0 reviews     Review now
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              Recessive symptomatic focal epilepsy and mutant contactin-associated protein-like 2.

              Kevin Strauss, Erik G. Puffenberger, Matthew J. Huentelman … (2006)
              Contactin-associated protein-like 2 (CASPR2) is encoded by CNTNAP2 and clusters voltage-gated potassium channels (K(v)1.1) at the nodes of Ranvier. We report a homozygous mutation of CNTNAP2 in Old Order Amish children with cortical dysplasia, focal epilepsy, relative macrocephaly, and diminished deep-tendon reflexes. Intractable focal seizures began in early childhood, after which language regression, hyperactivity, impulsive and aggressive behavior, and mental retardation developed in all children. Resective surgery did not prevent the recurrence of seizures. Temporal-lobe specimens showed evidence of abnormalities of neuronal migration and structure, widespread astrogliosis, and reduced expression of CASPR2. Copyright 2006 Massachusetts Medical Society.
              Article 0 comments Cited 177 times – based on 0 reviews     Review now
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                Author and article information

                Contributors
                Anna Dunaevsky: Role: Academic Editor
                Journal
                Journal ID (nlm-ta): PLoS One
                Journal ID (iso-abbrev): PLoS ONE
                Journal ID (publisher-id): plos
                Journal ID (pmc): plosone
                Title: PLoS ONE
                Publisher: Public Library of Science (San Francisco, CA USA )
                ISSN (Electronic): 1932-6203
                Publication date (Electronic): 7 May 2015
                Publication date Collection: 2015
                Volume: 10
                Issue: 5
                Electronic Location Identifier: e0125633
                Affiliations
                [1 ]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
                [2 ]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
                University of Nebraska Medical Center, UNITED STATES
                Author notes

                Competing Interests: The authors have declared that no competing interests exist.

                Conceived and designed the experiments: AG OP DG. Performed the experiments: AG OP. Analyzed the data: AG. Contributed reagents/materials/analysis tools: JTT. Wrote the paper: AG OP PG ML JTT DHG.

                [¤a]

                Current address: Department of Neurobiology, Tel Aviv University, Tel Aviv, Israel

                [¤b]

                Current address: Department of Pharmacology, School of Medicine, University of the Basque Country, Leioa, Bizkaia, Spain

                Article
                Publisher ID: PONE-D-14-52074
                DOI: 10.1371/journal.pone.0125633
                PMC ID: 4423902
                PubMed ID: 25951243
                SO-VID: 3b269c65-cf33-46e7-a613-f6a00cda17ac
                Copyright statement: Copyright @ 2015
                License:

                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 credited

                History
                Date received : 27 November 2014
                Date accepted : 18 March 2015
                Page count
                Figures: 2, Tables: 0, Pages: 7
                Funding
                This work was supported by ACE Network grant 5RO1MH081754 and the renewal RO1MH10027. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
                Categories
                Subject: Research Article
                Custom metadata
                Data Availability All data are available upon request from the corresponding author: amos.gdalyahu@ 123456gmail.com . The data may also be found at http://goo.gl/WPh6tu.

                ScienceOpen disciplines: Uncategorized
                Data availability:
                ScienceOpen disciplines: Uncategorized

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