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in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA
Titre : Mouse Behavior and Models for Autism Spectrum Disorders Type de document : Texte imprimé et/ou numérique Auteurs : Laura RICCERI, Auteur ; Caterina MICHETTI, Auteur ; Maria Luisa SCATTONI, Auteur Année de publication : 2016 Importance : p.269-293 Langues : Anglais (eng) Mots-clés : Mouse behavior Mouse models Mutants Olfactory tests Repetitive behaviors Social approach Social communication Social interaction Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Autism spectrum disorders (ASDs) are behaviorally defined disorders including attenuated or abnormal social interaction and communication, as well as aberrant repetitive behavior, with symptoms emerging early in childhood. Although the cause of autism has not been discovered, several data strongly support the role of genetic factors in its etiology. For this reason, preclinical research has focused on transgenic and knockout mice bearing mutations in genes identified in autistic children, with the aim of understanding the role of those genes in autism etiology, discovering the biological mechanisms underlying behavioral alterations observed and evaluating potential treatments. In past years, a number of behavioral phenotyping assays for rodent models of autism and related disorders have been developed. In the first part of our review, we describe these behavioral paradigms currently used in ASD rodent models; the second part is an overview of valid and robust animal models of ASD. En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00017-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 Mouse Behavior and Models for Autism Spectrum Disorders [Texte imprimé et/ou numérique] / Laura RICCERI, Auteur ; Caterina MICHETTI, Auteur ; Maria Luisa SCATTONI, Auteur . - 2016 . - p.269-293.
in Neuronal and Synaptic Dysfunction in Autism Spectrum Disorder and Intellectual Disability / Carlo SALA
Langues : Anglais (eng)
Mots-clés : Mouse behavior Mouse models Mutants Olfactory tests Repetitive behaviors Social approach Social communication Social interaction Index. décimale : SCI-D SCI-D - Neurosciences Résumé : Autism spectrum disorders (ASDs) are behaviorally defined disorders including attenuated or abnormal social interaction and communication, as well as aberrant repetitive behavior, with symptoms emerging early in childhood. Although the cause of autism has not been discovered, several data strongly support the role of genetic factors in its etiology. For this reason, preclinical research has focused on transgenic and knockout mice bearing mutations in genes identified in autistic children, with the aim of understanding the role of those genes in autism etiology, discovering the biological mechanisms underlying behavioral alterations observed and evaluating potential treatments. In past years, a number of behavioral phenotyping assays for rodent models of autism and related disorders have been developed. In the first part of our review, we describe these behavioral paradigms currently used in ASD rodent models; the second part is an overview of valid and robust animal models of ASD. En ligne : http://dx.doi.org/10.1016/B978-0-12-800109-7.00017-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=301 Exemplaires
Code-barres Cote Support Localisation Section Disponibilité aucun exemplaire A Novel Chd8 Mutant Mouse Displays Altered Ultrasonic Vocalizations and Enhanced Motor Coordination / Samuel W. HULBERT in Autism Research, 13-10 (October 2020)
[article]
Titre : A Novel Chd8 Mutant Mouse Displays Altered Ultrasonic Vocalizations and Enhanced Motor Coordination Type de document : Texte imprimé et/ou numérique Auteurs : Samuel W. HULBERT, Auteur ; Xiaoming WANG, Auteur ; Simisola O. GBADEGESIN, Auteur ; Qiong XU, Auteur ; Xiu XU, Auteur ; Yong-hui JIANG, Auteur Article en page(s) : p.1685-1697 Langues : Anglais (eng) Mots-clés : Asd Chd8 autism mouse behavior mouse models Index. décimale : PER Périodiques Résumé : Mutations in CHD8 are among the most common autism-causing genetic defects identified in human genomics studies. Therefore, many labs have attempted to model this disorder by generating mice with mutations in Chd8. Using a gene trap inserted after Exon 31, we created a novel Chd8 mutant mouse (Chd8(+/E31T) ) and characterized its behavior on several different assays thought to have face validity for the human condition, attempting to model both the core symptoms (repetitive behaviors and social communication impairments) and common comorbidities (motor deficits, anxiety, and intellectual disability). We found that Chd8(+/E31T) mice showed no difference compared to wild-type mice in amount of self-grooming, reproducing the negative finding most other studies have reported. Unlike some of the other published lines, Chd8(+/E31T) mice did not show deficits in the three-chamber test for social novelty preference. A few studies have examined ultrasonic vocalizations in Chd8 mutant mice, but we are the first to report an increase in call length for adult mice. Additionally, we found that in contrast to previous published lines, Chd8(+/E31T) mice displayed no anxiety-like behaviors or learning impairments but showed paradoxically significant improvement in motor function. The inconsistencies in behavioral phenotypes in the Chd8 mutant mice generated by different laboratories poses a challenge for modeling autism spectrum disorder and preclinical studies in mice going forward and warrants further investigation into the molecular consequences of the different mutations in Chd8 and the functional impact on behavior. LAY SUMMARY: Several different mouse models carrying mutations in the Chd8 gene have been created to study the effects of these autism-causing mutations in the laboratory. The current study characterizes a novel Chd8 mutant mouse model as well as summarizes data from previously published Chd8 mutant mice. The inconsistencies between different studies are concerning, but future research into the reasons why these inconsistencies occur may help us understand why patients with various mutations have different degrees of symptom severity. Autism Res 2020, 13: 1685-1697. © 2020 International Society for Autism Research and Wiley Periodicals LLC. En ligne : http://dx.doi.org/10.1002/aur.2353 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=431
in Autism Research > 13-10 (October 2020) . - p.1685-1697[article] A Novel Chd8 Mutant Mouse Displays Altered Ultrasonic Vocalizations and Enhanced Motor Coordination [Texte imprimé et/ou numérique] / Samuel W. HULBERT, Auteur ; Xiaoming WANG, Auteur ; Simisola O. GBADEGESIN, Auteur ; Qiong XU, Auteur ; Xiu XU, Auteur ; Yong-hui JIANG, Auteur . - p.1685-1697.
Langues : Anglais (eng)
in Autism Research > 13-10 (October 2020) . - p.1685-1697
Mots-clés : Asd Chd8 autism mouse behavior mouse models Index. décimale : PER Périodiques Résumé : Mutations in CHD8 are among the most common autism-causing genetic defects identified in human genomics studies. Therefore, many labs have attempted to model this disorder by generating mice with mutations in Chd8. Using a gene trap inserted after Exon 31, we created a novel Chd8 mutant mouse (Chd8(+/E31T) ) and characterized its behavior on several different assays thought to have face validity for the human condition, attempting to model both the core symptoms (repetitive behaviors and social communication impairments) and common comorbidities (motor deficits, anxiety, and intellectual disability). We found that Chd8(+/E31T) mice showed no difference compared to wild-type mice in amount of self-grooming, reproducing the negative finding most other studies have reported. Unlike some of the other published lines, Chd8(+/E31T) mice did not show deficits in the three-chamber test for social novelty preference. A few studies have examined ultrasonic vocalizations in Chd8 mutant mice, but we are the first to report an increase in call length for adult mice. Additionally, we found that in contrast to previous published lines, Chd8(+/E31T) mice displayed no anxiety-like behaviors or learning impairments but showed paradoxically significant improvement in motor function. The inconsistencies in behavioral phenotypes in the Chd8 mutant mice generated by different laboratories poses a challenge for modeling autism spectrum disorder and preclinical studies in mice going forward and warrants further investigation into the molecular consequences of the different mutations in Chd8 and the functional impact on behavior. LAY SUMMARY: Several different mouse models carrying mutations in the Chd8 gene have been created to study the effects of these autism-causing mutations in the laboratory. The current study characterizes a novel Chd8 mutant mouse model as well as summarizes data from previously published Chd8 mutant mice. The inconsistencies between different studies are concerning, but future research into the reasons why these inconsistencies occur may help us understand why patients with various mutations have different degrees of symptom severity. Autism Res 2020, 13: 1685-1697. © 2020 International Society for Autism Research and Wiley Periodicals LLC. En ligne : http://dx.doi.org/10.1002/aur.2353 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=431 CYFIP1 overexpression increases fear response in mice but does not affect social or repetitive behavioral phenotypes / C. FRICANO-KUGLER in Molecular Autism, 10 (2019)
[article]
Titre : CYFIP1 overexpression increases fear response in mice but does not affect social or repetitive behavioral phenotypes Type de document : Texte imprimé et/ou numérique Auteurs : C. FRICANO-KUGLER, Auteur ; A. GORDON, Auteur ; G. SHIN, Auteur ; K. GAO, Auteur ; J. NGUYEN, Auteur ; J. BERG, Auteur ; M. STARKS, Auteur ; D. H. GESCHWIND, Auteur Article en page(s) : 25p. Langues : Anglais (eng) Mots-clés : Autism spectrum disorder (ASD) Cyfip1 Dup15q Fear conditioning Mouse behavior Neurodevelopmental disorders RNA sequencing Index. décimale : PER Périodiques Résumé : Background: CYFIP1, a protein that interacts with FMRP and regulates protein synthesis and actin dynamics, is overexpressed in Dup15q syndrome as well as autism spectrum disorder (ASD). While CYFIP1 heterozygosity has been rigorously studied due to its loss in 15q11.2 deletion, Prader-Willi and Angelman syndrome, the effects of CYFIP1 overexpression, as is observed in patients with CYFIP1 duplication, are less well understood. Methods: We developed and validated a mouse model of human CYFIP1 overexpression (CYFIP1 OE) using qPCR and western blot analysis. We performed a large battery of behavior testing on these mice, including ultrasonic vocalizations, three-chamber social assay, home-cage behavior, Y-maze, elevated plus maze, open field test, Morris water maze, fear conditioning, prepulse inhibition, and the hot plate assay. We also performed RNA sequencing and analysis on the basolateral amygdala. Results: Extensive behavioral testing in CYFIP1 OE mice reveals no changes in the core behaviors related to ASD: social interactions and repetitive behaviors. However, we did observe mild learning deficits and an exaggerated fear response. Using RNA sequencing of the basolateral amygdala, a region associated with fear response, we observed changes in pathways related to cytoskeletal regulation, oligodendrocytes, and myelination. We also identified GABA-A subunit composition changes in basolateral amygdala neurons, which are essential components of the neural fear conditioning circuit. Conclusion: Overall, this research identifies the behavioral and molecular consequences of CYFIP1 overexpression and how they contribute to the variable phenotype seen in Dup15q syndrome and in ASD patients with excess CYFIP1. En ligne : http://dx.doi.org/10.1186/s13229-019-0278-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402
in Molecular Autism > 10 (2019) . - 25p.[article] CYFIP1 overexpression increases fear response in mice but does not affect social or repetitive behavioral phenotypes [Texte imprimé et/ou numérique] / C. FRICANO-KUGLER, Auteur ; A. GORDON, Auteur ; G. SHIN, Auteur ; K. GAO, Auteur ; J. NGUYEN, Auteur ; J. BERG, Auteur ; M. STARKS, Auteur ; D. H. GESCHWIND, Auteur . - 25p.
Langues : Anglais (eng)
in Molecular Autism > 10 (2019) . - 25p.
Mots-clés : Autism spectrum disorder (ASD) Cyfip1 Dup15q Fear conditioning Mouse behavior Neurodevelopmental disorders RNA sequencing Index. décimale : PER Périodiques Résumé : Background: CYFIP1, a protein that interacts with FMRP and regulates protein synthesis and actin dynamics, is overexpressed in Dup15q syndrome as well as autism spectrum disorder (ASD). While CYFIP1 heterozygosity has been rigorously studied due to its loss in 15q11.2 deletion, Prader-Willi and Angelman syndrome, the effects of CYFIP1 overexpression, as is observed in patients with CYFIP1 duplication, are less well understood. Methods: We developed and validated a mouse model of human CYFIP1 overexpression (CYFIP1 OE) using qPCR and western blot analysis. We performed a large battery of behavior testing on these mice, including ultrasonic vocalizations, three-chamber social assay, home-cage behavior, Y-maze, elevated plus maze, open field test, Morris water maze, fear conditioning, prepulse inhibition, and the hot plate assay. We also performed RNA sequencing and analysis on the basolateral amygdala. Results: Extensive behavioral testing in CYFIP1 OE mice reveals no changes in the core behaviors related to ASD: social interactions and repetitive behaviors. However, we did observe mild learning deficits and an exaggerated fear response. Using RNA sequencing of the basolateral amygdala, a region associated with fear response, we observed changes in pathways related to cytoskeletal regulation, oligodendrocytes, and myelination. We also identified GABA-A subunit composition changes in basolateral amygdala neurons, which are essential components of the neural fear conditioning circuit. Conclusion: Overall, this research identifies the behavioral and molecular consequences of CYFIP1 overexpression and how they contribute to the variable phenotype seen in Dup15q syndrome and in ASD patients with excess CYFIP1. En ligne : http://dx.doi.org/10.1186/s13229-019-0278-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=402