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
-
Détail de l'auteur
Auteur Sheryl S. MOY |
Documents disponibles écrits par cet auteur (2)
Faire une suggestion Affiner la recherche
Early life sleep disruption potentiates lasting sex-specific changes in behavior in genetically vulnerable Shank3 heterozygous autism model mice / Julia S. LORD in Molecular Autism, 13 (2022)
[article]
Titre : Early life sleep disruption potentiates lasting sex-specific changes in behavior in genetically vulnerable Shank3 heterozygous autism model mice Type de document : Texte imprimé et/ou numérique Auteurs : Julia S. LORD, Auteur ; Sean M. GAY, Auteur ; Kathryn M. HARPER, Auteur ; Viktoriya D. NIKOLOVA, Auteur ; Kirsten M. SMITH, Auteur ; Sheryl S. MOY, Auteur ; Graham H. DIERING, Auteur Article en page(s) : 35 p. Langues : Anglais (eng) Mots-clés : Animals Autism Spectrum Disorder/genetics Autistic Disorder/genetics Disease Models, Animal Female Male Mice Microfilament Proteins Nerve Tissue Proteins/genetics Sleep Autism spectrum disorder Brain development Shank3 Social behavior Index. décimale : PER Périodiques Résumé : BACKGROUND: Patients with autism spectrum disorder (ASD) experience high rates of sleep disruption beginning early in life; however, the developmental consequences of this disruption are not understood. We examined sleep behavior and the consequences of sleep disruption in developing mice bearing C-terminal truncation mutation in the high-confidence ASD risk gene SHANK3 (Shank3ΔC). We hypothesized that sleep disruption may be an early sign of developmental divergence, and that clinically relevant Shank3(WT/ΔC) mice may be at increased risk of lasting deleterious outcomes following early life sleep disruption. METHODS: We recorded sleep behavior in developing Shank3(ΔC/ΔC), Shank3(WT/ΔC), and wild-type siblings of both sexes using a noninvasive home-cage monitoring system. Separately, litters of Shank3(WT/ΔC) and wild-type littermates were exposed to automated mechanical sleep disruption for 7 days prior to weaning (early life sleep disruption: ELSD) or post-adolescence (PASD) or undisturbed control (CON) conditions. All groups underwent standard behavioral testing as adults. RESULTS: Male and female Shank3(ΔC/ΔC) mice slept significantly less than wild-type and Shank3(WT/ΔC) siblings shortly after weaning, with increasing sleep fragmentation in adolescence, indicating that sleep disruption has a developmental onset in this ASD model. ELSD treatment interacted with genetic vulnerability in Shank3(WT/ΔC) mice, resulting in lasting, sex-specific changes in behavior, whereas wild-type siblings were largely resilient to these effects. Male ELSD Shank3(WT/ΔC) subjects demonstrated significant changes in sociability, sensory processing, and locomotion, while female ELSD Shank3(WT/ΔC) subjects had a significant reduction in risk aversion. CON Shank3(WT/ΔC) mice, PASD mice, and all wild-type mice demonstrated typical behavioral responses in most tests. LIMITATIONS: This study tested the interaction between developmental sleep disruption and genetic vulnerability using a single ASD mouse model: Shank3ΔC (deletion of exon 21). The broader implications of this work should be supported by additional studies using ASD model mice with distinct genetic vulnerabilities. CONCLUSION: Our study shows that sleep disruption during sensitive periods of early life interacts with underlying genetic vulnerability to drive lasting and sex-specific changes in behavior. As individuals progress through maturation, they gain resilience to the lasting effects of sleep disruption. This work highlights developmental sleep disruption as an important vulnerability in ASD susceptibility. En ligne : http://dx.doi.org/10.1186/s13229-022-00514-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=491
in Molecular Autism > 13 (2022) . - 35 p.[article] Early life sleep disruption potentiates lasting sex-specific changes in behavior in genetically vulnerable Shank3 heterozygous autism model mice [Texte imprimé et/ou numérique] / Julia S. LORD, Auteur ; Sean M. GAY, Auteur ; Kathryn M. HARPER, Auteur ; Viktoriya D. NIKOLOVA, Auteur ; Kirsten M. SMITH, Auteur ; Sheryl S. MOY, Auteur ; Graham H. DIERING, Auteur . - 35 p.
Langues : Anglais (eng)
in Molecular Autism > 13 (2022) . - 35 p.
Mots-clés : Animals Autism Spectrum Disorder/genetics Autistic Disorder/genetics Disease Models, Animal Female Male Mice Microfilament Proteins Nerve Tissue Proteins/genetics Sleep Autism spectrum disorder Brain development Shank3 Social behavior Index. décimale : PER Périodiques Résumé : BACKGROUND: Patients with autism spectrum disorder (ASD) experience high rates of sleep disruption beginning early in life; however, the developmental consequences of this disruption are not understood. We examined sleep behavior and the consequences of sleep disruption in developing mice bearing C-terminal truncation mutation in the high-confidence ASD risk gene SHANK3 (Shank3ΔC). We hypothesized that sleep disruption may be an early sign of developmental divergence, and that clinically relevant Shank3(WT/ΔC) mice may be at increased risk of lasting deleterious outcomes following early life sleep disruption. METHODS: We recorded sleep behavior in developing Shank3(ΔC/ΔC), Shank3(WT/ΔC), and wild-type siblings of both sexes using a noninvasive home-cage monitoring system. Separately, litters of Shank3(WT/ΔC) and wild-type littermates were exposed to automated mechanical sleep disruption for 7 days prior to weaning (early life sleep disruption: ELSD) or post-adolescence (PASD) or undisturbed control (CON) conditions. All groups underwent standard behavioral testing as adults. RESULTS: Male and female Shank3(ΔC/ΔC) mice slept significantly less than wild-type and Shank3(WT/ΔC) siblings shortly after weaning, with increasing sleep fragmentation in adolescence, indicating that sleep disruption has a developmental onset in this ASD model. ELSD treatment interacted with genetic vulnerability in Shank3(WT/ΔC) mice, resulting in lasting, sex-specific changes in behavior, whereas wild-type siblings were largely resilient to these effects. Male ELSD Shank3(WT/ΔC) subjects demonstrated significant changes in sociability, sensory processing, and locomotion, while female ELSD Shank3(WT/ΔC) subjects had a significant reduction in risk aversion. CON Shank3(WT/ΔC) mice, PASD mice, and all wild-type mice demonstrated typical behavioral responses in most tests. LIMITATIONS: This study tested the interaction between developmental sleep disruption and genetic vulnerability using a single ASD mouse model: Shank3ΔC (deletion of exon 21). The broader implications of this work should be supported by additional studies using ASD model mice with distinct genetic vulnerabilities. CONCLUSION: Our study shows that sleep disruption during sensitive periods of early life interacts with underlying genetic vulnerability to drive lasting and sex-specific changes in behavior. As individuals progress through maturation, they gain resilience to the lasting effects of sleep disruption. This work highlights developmental sleep disruption as an important vulnerability in ASD susceptibility. En ligne : http://dx.doi.org/10.1186/s13229-022-00514-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=491 Mouse Behavioral Models for Autism Spectrum Disorders / William C. WETSEL
Titre : Mouse Behavioral Models for Autism Spectrum Disorders Type de document : Texte imprimé et/ou numérique Auteurs : William C. WETSEL, Auteur ; Sheryl S. MOY, Auteur ; Yong-hui JIANG, Auteur Année de publication : 2013 Importance : p.363-378 Langues : Anglais (eng) Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Autism spectrum disorders (ASD) involve impaired development of social interaction and communication, as well as restricted, repetitive, and stereotyped behaviors. ASD has high heritability and certain chromosomal regions and at risk genes are associated with the conditions. Experiments with inbred and outbred rodent models of ASD have revealed procedures that can partially or fully rescue the phenotype; metabotropic GluR5 antagonists appear especially promising in certain models. We summarize behavioral approaches for analyzing mouse models for ASD and review studies in Shank3 mice as a specific example. As SHANK3 variants are identified as a risk factor for autism, mouse lines have been developed with deletions in exons 4–9, exons 13–16, and exon 21 that display, to varying degrees, ASD-like behaviors. Future research with Shank3 lines and other genetic models should help determine the mechanistic basis for both core symptomatologies and divergent behavioral profiles in ASD. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189 Mouse Behavioral Models for Autism Spectrum Disorders [Texte imprimé et/ou numérique] / William C. WETSEL, Auteur ; Sheryl S. MOY, Auteur ; Yong-hui JIANG, Auteur . - 2013 . - p.363-378.
Langues : Anglais (eng)
Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Autism spectrum disorders (ASD) involve impaired development of social interaction and communication, as well as restricted, repetitive, and stereotyped behaviors. ASD has high heritability and certain chromosomal regions and at risk genes are associated with the conditions. Experiments with inbred and outbred rodent models of ASD have revealed procedures that can partially or fully rescue the phenotype; metabotropic GluR5 antagonists appear especially promising in certain models. We summarize behavioral approaches for analyzing mouse models for ASD and review studies in Shank3 mice as a specific example. As SHANK3 variants are identified as a risk factor for autism, mouse lines have been developed with deletions in exons 4–9, exons 13–16, and exon 21 that display, to varying degrees, ASD-like behaviors. Future research with Shank3 lines and other genetic models should help determine the mechanistic basis for both core symptomatologies and divergent behavioral profiles in ASD. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=189 Exemplaires
Code-barres Cote Support Localisation Section Disponibilité aucun exemplaire