Correction: Differentially altered social dominance- and cooperative-like behaviors in Shank2- and Shank3-mutant mice / Kyung Ah HAN in Molecular Autism, 15 (2024)  

Public ISBD [article]  inMolecular Autism > 15 (2024) . - 32p. Titre : Correction: Differentially altered social dominance- and cooperative-like behaviors in Shank2- and Shank3-mutant mice Type de document : Texte imprimé et/ou numérique Auteurs : Kyung Ah HAN, Auteur ; Taek Han YOON, Auteur ; Jungsu SHIN, Auteur ; Ji Won UM, Auteur ; Jaewon KO, Auteur Article en page(s) : 32p. Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : https://dx.doi.org/10.1186/s13229-024-00612-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538 [article] Correction: Differentially altered social dominance- and cooperative-like behaviors in Shank2- and Shank3-mutant mice [Texte imprimé et/ou numérique] / Kyung Ah HAN, Auteur ; Taek Han YOON, Auteur ; Jungsu SHIN, Auteur ; Ji Won UM, Auteur ; Jaewon KO, Auteur . - 32p. Langues : Anglais (eng) in Molecular Autism > 15 (2024) . - 32p. Index. décimale : PER Périodiques En ligne : https://dx.doi.org/10.1186/s13229-024-00612-6 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538

Differentially altered social dominance- and cooperative-like behaviors in Shank2- and Shank3-mutant mice / Kyung Ah HAN in Molecular Autism, 11 (2020)  

Public ISBD [article]  inMolecular Autism > 11 (2020) Titre : Differentially altered social dominance- and cooperative-like behaviors in Shank2- and Shank3-mutant mice Type de document : Texte imprimé et/ou numérique Auteurs : Kyung Ah HAN, Auteur ; Taek Han YOON, Auteur ; Jungsu SHIN, Auteur ; Ji Won UM, Auteur ; Jaewon KO, Auteur Langues : Anglais (eng) Mots-clés : Autism  Shank2  Shank3  Social cooperation  Social dominance  Tube test Index. décimale : PER Périodiques Résumé : BACKGROUND: Recent progress in genomics has contributed to the identification of a large number of autism spectrum disorder (ASD) risk genes, many of which encode synaptic proteins. Our understanding of ASDs has advanced rapidly, partly owing to the development of numerous animal models. Extensive characterizations using a variety of behavioral batteries that analyze social behaviors have shown that a subset of engineered mice that model mutations in genes encoding Shanks, a family of excitatory postsynaptic scaffolding proteins, exhibit autism-like behaviors. Although these behavioral assays have been useful in identifying deficits in simple social behaviors, alterations in complex social behaviors remain largely untested. METHODS: Two syndromic ASD mouse models-Shank2 constitutive knockout [KO] mice and Shank3 constitutive KO mice-were examined for alterations in social dominance and social cooperative behaviors using tube tests and automated cooperation tests. Upon naïve and salient behavioral experience, expression levels of c-Fos were analyzed as a proxy for neural activity across diverse brain areas, including the medial prefrontal cortex (mPFC) and a number of subcortical structures. FINDINGS: As previously reported, Shank2 KO mice showed deficits in sociability, with intact social recognition memory, whereas Shank3 KO mice displayed no overt phenotypes. Strikingly, the two Shank KO mouse models exhibited diametrically opposed alterations in social dominance and cooperative behaviors. After a specific social behavioral experience, Shank mutant mice exhibited distinct changes in number of c-Fos(+) neurons in the number of cortical and subcortical brain regions. CONCLUSIONS: Our results underscore the heterogeneity of social behavioral alterations in different ASD mouse models and highlight the utility of testing complex social behaviors in validating neurodevelopmental and neuropsychiatric disorder models. In addition, neural activities at distinct brain regions are likely collectively involved in eliciting complex social behaviors, which are differentially altered in ASD mouse models. En ligne : http://dx.doi.org/10.1186/s13229-020-00392-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438 [article] Differentially altered social dominance- and cooperative-like behaviors in Shank2- and Shank3-mutant mice [Texte imprimé et/ou numérique] / Kyung Ah HAN, Auteur ; Taek Han YOON, Auteur ; Jungsu SHIN, Auteur ; Ji Won UM, Auteur ; Jaewon KO, Auteur. Langues : Anglais (eng) in Molecular Autism > 11 (2020) Mots-clés : Autism  Shank2  Shank3  Social cooperation  Social dominance  Tube test Index. décimale : PER Périodiques Résumé : BACKGROUND: Recent progress in genomics has contributed to the identification of a large number of autism spectrum disorder (ASD) risk genes, many of which encode synaptic proteins. Our understanding of ASDs has advanced rapidly, partly owing to the development of numerous animal models. Extensive characterizations using a variety of behavioral batteries that analyze social behaviors have shown that a subset of engineered mice that model mutations in genes encoding Shanks, a family of excitatory postsynaptic scaffolding proteins, exhibit autism-like behaviors. Although these behavioral assays have been useful in identifying deficits in simple social behaviors, alterations in complex social behaviors remain largely untested. METHODS: Two syndromic ASD mouse models-Shank2 constitutive knockout [KO] mice and Shank3 constitutive KO mice-were examined for alterations in social dominance and social cooperative behaviors using tube tests and automated cooperation tests. Upon naïve and salient behavioral experience, expression levels of c-Fos were analyzed as a proxy for neural activity across diverse brain areas, including the medial prefrontal cortex (mPFC) and a number of subcortical structures. FINDINGS: As previously reported, Shank2 KO mice showed deficits in sociability, with intact social recognition memory, whereas Shank3 KO mice displayed no overt phenotypes. Strikingly, the two Shank KO mouse models exhibited diametrically opposed alterations in social dominance and cooperative behaviors. After a specific social behavioral experience, Shank mutant mice exhibited distinct changes in number of c-Fos(+) neurons in the number of cortical and subcortical brain regions. CONCLUSIONS: Our results underscore the heterogeneity of social behavioral alterations in different ASD mouse models and highlight the utility of testing complex social behaviors in validating neurodevelopmental and neuropsychiatric disorder models. In addition, neural activities at distinct brain regions are likely collectively involved in eliciting complex social behaviors, which are differentially altered in ASD mouse models. En ligne : http://dx.doi.org/10.1186/s13229-020-00392-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438

Mutations in Synaptic Adhesion Molecules / Jaewon KO  

Public ISBD in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA Titre : Mutations in Synaptic Adhesion Molecules Type de document : Texte imprimé et/ou numérique Auteurs : Jaewon KO, Auteur ; Caterina MONTANI, Auteur ; Eunjoon KIM, Auteur ; Carlo SALA, Auteur Année de publication : 2016 Importance : p.161-175 Langues : Anglais (eng) Mots-clés : Excitatory synapse  Inhibitory synapse  Neurodevelopmental diseases  Postsynaptic density  Presynapse  Synapse formation Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Synaptic connections are established between neurons during development of the nervous system after axon path finding and dendrite development. Synapse development is mediated by specific synaptic cell adhesion molecules (SCAMs) that accumulate at pre- and postsynaptic sites and trigger synaptic differentiation through interactions with intra- and extracellular proteins. These interactions are essential to align pre- and postsynaptic specializations and to couple the sites of cell-to-cell adhesion to the cytoskeletal and signaling complexes required to recruit and recycle presynaptic vesicles, components of exo- and endocytic zones, and postsynaptic receptors. Not surprisingly, it has been demonstrated that in humans, deletions or mutations in some of the SCAM genes are associated with several neurodevelopmental disorders, including autism spectrum disorders, intellectual disability, and schizophrenia, although the exact connection between genetic background and biochemical mechanisms by which these mutations contribute to the diseases has been only partially revealed. This chapter describes the multiple functions and associated synaptic alterations of the SCAM genes found mutated in neurodevelopmental diseases. En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00011-X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA Mutations in Synaptic Adhesion Molecules [Texte imprimé et/ou numérique] / Jaewon KO, Auteur ; Caterina MONTANI, Auteur ; Eunjoon KIM, Auteur ; Carlo SALA, Auteur . - 2016 . - p.161-175. Langues : Anglais (eng) Mots-clés : Excitatory synapse  Inhibitory synapse  Neurodevelopmental diseases  Postsynaptic density  Presynapse  Synapse formation Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Synaptic connections are established between neurons during development of the nervous system after axon path finding and dendrite development. Synapse development is mediated by specific synaptic cell adhesion molecules (SCAMs) that accumulate at pre- and postsynaptic sites and trigger synaptic differentiation through interactions with intra- and extracellular proteins. These interactions are essential to align pre- and postsynaptic specializations and to couple the sites of cell-to-cell adhesion to the cytoskeletal and signaling complexes required to recruit and recycle presynaptic vesicles, components of exo- and endocytic zones, and postsynaptic receptors. Not surprisingly, it has been demonstrated that in humans, deletions or mutations in some of the SCAM genes are associated with several neurodevelopmental disorders, including autism spectrum disorders, intellectual disability, and schizophrenia, although the exact connection between genetic background and biochemical mechanisms by which these mutations contribute to the diseases has been only partially revealed. This chapter describes the multiple functions and associated synaptic alterations of the SCAM genes found mutated in neurodevelopmental diseases. En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00011-X Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301

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