Centre d'Information et de documentation du CRA Rhône-Alpes
CRA
Informations pratiques
-
Adresse
Centre d'information et de documentation
du CRA Rhône-Alpes
Centre Hospitalier le Vinatier
bât 211
95, Bd Pinel
69678 Bron CedexHoraires
Lundi au Vendredi
9h00-12h00 13h30-16h00Contact
Tél: +33(0)4 37 91 54 65
Mail
Fax: +33(0)4 37 91 54 37
-
Résultat de la recherche
3 recherche sur le mot-clé 'Social dominance'
Affiner la recherche Générer le flux rss de la recherche
Partager le résultat de cette recherche Faire une suggestion
Differentially altered social dominance- and cooperative-like behaviors in Shank2- and Shank3-mutant mice / Kyung Ah HAN in Molecular Autism, 11 (2020)
[article]
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
in Molecular Autism > 11 (2020)[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 MEK inhibition ameliorates social behavior phenotypes in a Spred1 knockout mouse model for RASopathy disorders / S. C. BORRIE in Molecular Autism, 12 (2021)
[article]
Titre : MEK inhibition ameliorates social behavior phenotypes in a Spred1 knockout mouse model for RASopathy disorders Type de document : Texte imprimé et/ou numérique Auteurs : S. C. BORRIE, Auteur ; E. PLASSCHAERT, Auteur ; Z. CALLAERTS-VEGH, Auteur ; A. YOSHIMURA, Auteur ; R. D'HOOGE, Auteur ; Y. ELGERSMA, Auteur ; S. A. KUSHNER, Auteur ; E. LEGIUS, Auteur ; H. BREMS, Auteur Article en page(s) : 53 p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder Neurofibromatosis type 1 RASopathy Social dominance Spred1 Ultrasonic vocalization declare no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: RASopathies are a group of disorders that result from mutations in genes coding for proteins involved in regulating the Ras-MAPK signaling pathway, and have an increased incidence of autism spectrum disorder (ASD). Legius syndrome is a rare RASopathy caused by loss-of-function mutations in the SPRED1 gene. The patient phenotype is similar to, but milder than, Neurofibromatosis type 1-another RASopathy caused by loss-of-function mutations in the NF1 gene. RASopathies exhibit increased activation of Ras-MAPK signaling and commonly manifest with cognitive impairments and ASD. Here, we investigated if a Spred1-/- mouse model for Legius syndrome recapitulates ASD-like symptoms, and whether targeting the Ras-MAPK pathway has therapeutic potential in this RASopathy mouse model. METHODS: We investigated social and communicative behaviors in Spred1-/- mice and probed therapeutic mechanisms underlying the observed behavioral phenotypes by pharmacological targeting of the Ras-MAPK pathway with the MEK inhibitor PD325901. RESULTS: Spred1-/- mice have robust increases in social dominance in the automated tube test and reduced adult ultrasonic vocalizations during social communication. Neonatal ultrasonic vocalization was also altered, with significant differences in spectral properties. Spred1-/- mice also exhibit impaired nesting behavior. Acute MEK inhibitor treatment in adulthood with PD325901 reversed the enhanced social dominance in Spred1-/- mice to normal levels, and improved nesting behavior in adult Spred1-/- mice. LIMITATIONS: This study used an acute treatment protocol to administer the drug. It is not known what the effects of longer-term treatment would be on behavior. Further studies titrating the lowest dose of this drug that is required to alter Spred1-/- social behavior are still required. Finally, our findings are in a homozygous mouse model, whereas patients carry heterozygous mutations. These factors should be considered before any translational conclusions are drawn. CONCLUSIONS: These results demonstrate for the first time that social behavior phenotypes in a mouse model for RASopathies (Spred1-/-) can be acutely reversed. This highlights a key role for Ras-MAPK dysregulation in mediating social behavior phenotypes in mouse models for ASD, suggesting that proper regulation of Ras-MAPK signaling is important for social behavior. En ligne : http://dx.doi.org/10.1186/s13229-021-00458-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459
in Molecular Autism > 12 (2021) . - 53 p.[article] MEK inhibition ameliorates social behavior phenotypes in a Spred1 knockout mouse model for RASopathy disorders [Texte imprimé et/ou numérique] / S. C. BORRIE, Auteur ; E. PLASSCHAERT, Auteur ; Z. CALLAERTS-VEGH, Auteur ; A. YOSHIMURA, Auteur ; R. D'HOOGE, Auteur ; Y. ELGERSMA, Auteur ; S. A. KUSHNER, Auteur ; E. LEGIUS, Auteur ; H. BREMS, Auteur . - 53 p.
Langues : Anglais (eng)
in Molecular Autism > 12 (2021) . - 53 p.
Mots-clés : Autism spectrum disorder Neurofibromatosis type 1 RASopathy Social dominance Spred1 Ultrasonic vocalization declare no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: RASopathies are a group of disorders that result from mutations in genes coding for proteins involved in regulating the Ras-MAPK signaling pathway, and have an increased incidence of autism spectrum disorder (ASD). Legius syndrome is a rare RASopathy caused by loss-of-function mutations in the SPRED1 gene. The patient phenotype is similar to, but milder than, Neurofibromatosis type 1-another RASopathy caused by loss-of-function mutations in the NF1 gene. RASopathies exhibit increased activation of Ras-MAPK signaling and commonly manifest with cognitive impairments and ASD. Here, we investigated if a Spred1-/- mouse model for Legius syndrome recapitulates ASD-like symptoms, and whether targeting the Ras-MAPK pathway has therapeutic potential in this RASopathy mouse model. METHODS: We investigated social and communicative behaviors in Spred1-/- mice and probed therapeutic mechanisms underlying the observed behavioral phenotypes by pharmacological targeting of the Ras-MAPK pathway with the MEK inhibitor PD325901. RESULTS: Spred1-/- mice have robust increases in social dominance in the automated tube test and reduced adult ultrasonic vocalizations during social communication. Neonatal ultrasonic vocalization was also altered, with significant differences in spectral properties. Spred1-/- mice also exhibit impaired nesting behavior. Acute MEK inhibitor treatment in adulthood with PD325901 reversed the enhanced social dominance in Spred1-/- mice to normal levels, and improved nesting behavior in adult Spred1-/- mice. LIMITATIONS: This study used an acute treatment protocol to administer the drug. It is not known what the effects of longer-term treatment would be on behavior. Further studies titrating the lowest dose of this drug that is required to alter Spred1-/- social behavior are still required. Finally, our findings are in a homozygous mouse model, whereas patients carry heterozygous mutations. These factors should be considered before any translational conclusions are drawn. CONCLUSIONS: These results demonstrate for the first time that social behavior phenotypes in a mouse model for RASopathies (Spred1-/-) can be acutely reversed. This highlights a key role for Ras-MAPK dysregulation in mediating social behavior phenotypes in mouse models for ASD, suggesting that proper regulation of Ras-MAPK signaling is important for social behavior. En ligne : http://dx.doi.org/10.1186/s13229-021-00458-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=459 Visualization and Analysis of Eye Movement Data from Children with Typical and Atypical Development / Terje FALCK-YTTER in Journal of Autism and Developmental Disorders, 43-10 (October 2013)
[article]
Titre : Visualization and Analysis of Eye Movement Data from Children with Typical and Atypical Development Type de document : Texte imprimé et/ou numérique Auteurs : Terje FALCK-YTTER, Auteur ; Claes HOFSTEN, Auteur ; Christopher GILLBERG, Auteur ; Elisabeth FERNELL, Auteur Article en page(s) : p.2249-2258 Langues : Anglais (eng) Mots-clés : Learning Eye tracking Scientific visualization Bottom-up Knowledge generation Autism spectrum disorder Diagnosis Attention Social dominance Social hierarchies Conflict Goals Index. décimale : PER Périodiques Résumé : Looking at other children’s interactions provides rich learning opportunities for a small child. How children with autism look at other children is largely unknown. Using eye tracking, we studied gaze performance in children with autism and neurotypical comparison children while they were watching videos of semi-naturalistic social interactions between young children. Using a novel, bottom-up approach we identified event-related measures that distinguished between groups with high accuracy. The observed effects remained in a subset of the total sample matched on IQ, and were replicated across several different stimuli. The described method facilitates the detection of meaningful patterns in complex eye tracking data. Also, the approach significantly improves visualization, which will help investigators understand, illustrate, and generate new hypotheses. En ligne : http://dx.doi.org/10.1007/s10803-013-1776-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=215
in Journal of Autism and Developmental Disorders > 43-10 (October 2013) . - p.2249-2258[article] Visualization and Analysis of Eye Movement Data from Children with Typical and Atypical Development [Texte imprimé et/ou numérique] / Terje FALCK-YTTER, Auteur ; Claes HOFSTEN, Auteur ; Christopher GILLBERG, Auteur ; Elisabeth FERNELL, Auteur . - p.2249-2258.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 43-10 (October 2013) . - p.2249-2258
Mots-clés : Learning Eye tracking Scientific visualization Bottom-up Knowledge generation Autism spectrum disorder Diagnosis Attention Social dominance Social hierarchies Conflict Goals Index. décimale : PER Périodiques Résumé : Looking at other children’s interactions provides rich learning opportunities for a small child. How children with autism look at other children is largely unknown. Using eye tracking, we studied gaze performance in children with autism and neurotypical comparison children while they were watching videos of semi-naturalistic social interactions between young children. Using a novel, bottom-up approach we identified event-related measures that distinguished between groups with high accuracy. The observed effects remained in a subset of the total sample matched on IQ, and were replicated across several different stimuli. The described method facilitates the detection of meaningful patterns in complex eye tracking data. Also, the approach significantly improves visualization, which will help investigators understand, illustrate, and generate new hypotheses. En ligne : http://dx.doi.org/10.1007/s10803-013-1776-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=215