Altered social behavior and ultrasonic communication in the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy / Rubén MIRANDA in Molecular Autism, (October 2015)  

Public ISBD [article]  inMolecular Autism > (October 2015) . - p.1-17 Titre : Altered social behavior and ultrasonic communication in the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy Type de document : Texte imprimé et/ou numérique Auteurs : Rubén MIRANDA, Auteur ; Flora NAGAPIN, Auteur ; Bruno BOZON, Auteur ; Serge LAROCHE, Auteur ; Thierry AUBIN, Auteur ; Cyrille VAILLEND, Auteur Article en page(s) : p.1-17 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : The Duchenne and Becker muscular dystrophies (DMD, BMD) show significant comorbid diagnosis for autism, and the genomic sequences encoding the proteins responsible for these diseases, the dystrophin and associated proteins, have been proposed as new candidate risk loci for autism. Dystrophin is expressed not only in muscles but also in central inhibitory synapses in the cerebellum, hippocampus, amygdala, and cerebral cortex, where it contributes to the organization of autism-associated trans-synaptic neurexin-neuroligin complexes and to the clustering of synaptic gamma-aminobutyric acid (GABA)A receptors. While brain defects due to dystrophin loss are associated with deficits in cognitive and executive functions, communication skills and social behavior, only a subpopulation of DMD patients meet the criteria for autism, suggesting that mutations in the dystrophin gene may confer a vulnerability to autism. The loss of dystrophin in the mdx mouse model of DMD has been associated with cognitive and emotional alterations, but social behavior and communication abilities have never been studied in this model. En ligne : http://dx.doi.org/10.1186/s13229-015-0053-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277 [article] Altered social behavior and ultrasonic communication in the dystrophin-deficient mdx mouse model of Duchenne muscular dystrophy [Texte imprimé et/ou numérique] / Rubén MIRANDA, Auteur ; Flora NAGAPIN, Auteur ; Bruno BOZON, Auteur ; Serge LAROCHE, Auteur ; Thierry AUBIN, Auteur ; Cyrille VAILLEND, Auteur . - p.1-17. Langues : Anglais (eng) in Molecular Autism > (October 2015) . - p.1-17 Index. décimale : PER Périodiques Résumé : The Duchenne and Becker muscular dystrophies (DMD, BMD) show significant comorbid diagnosis for autism, and the genomic sequences encoding the proteins responsible for these diseases, the dystrophin and associated proteins, have been proposed as new candidate risk loci for autism. Dystrophin is expressed not only in muscles but also in central inhibitory synapses in the cerebellum, hippocampus, amygdala, and cerebral cortex, where it contributes to the organization of autism-associated trans-synaptic neurexin-neuroligin complexes and to the clustering of synaptic gamma-aminobutyric acid (GABA)A receptors. While brain defects due to dystrophin loss are associated with deficits in cognitive and executive functions, communication skills and social behavior, only a subpopulation of DMD patients meet the criteria for autism, suggesting that mutations in the dystrophin gene may confer a vulnerability to autism. The loss of dystrophin in the mdx mouse model of DMD has been associated with cognitive and emotional alterations, but social behavior and communication abilities have never been studied in this model. En ligne : http://dx.doi.org/10.1186/s13229-015-0053-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=277

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