Dépouillements

Modeling Restricted Repetitive Behavior in Animals / Allison BECHARD in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 8 p. Titre : Modeling Restricted Repetitive Behavior in Animals Type de document : Texte imprimé et/ou numérique Auteurs : Allison BECHARD, Auteur ; Mark LEWIS, Auteur Article en page(s) : 8 p. Langues : Anglais (eng) Mots-clés : Repetitive behavior  Stereotypy  Cortical-basal ganglia circuitry  Autism spectrum disorders Index. décimale : PER Périodiques Résumé : Restricted, repetitive behavior is one of the three diagnostic domains for autism spectrum disorders, and commonly observed in a number of other neurodevelopmental disorders. Despite its clinical significance, effective treatments for restricted, repetitive behavior are limited including few, if any, pharmacological interventions with demonstrated efficacy. This is in large measure due to the lack of knowledge of the pathophysiological mechanisms that mediate the development and expression of repetitive behaviors in autism spectrum disorders. Therefore, animal models, particularly those that encompass both lower order and higher order repetitive behaviors, could be particularly useful. Such models could identify various potential etiologies, characterize commonalities in pathophysiology, identify novel potential therapeutic targets, and guide the development and validation of novel treatments. We have organized existing models of restricted, repetitive behavior in animals into four different categories: repetitive behavior resulting from a specific CNS insult (e.g. genetic mutation); repetitive behavior induced by specific pharmacological agents (e.g. amphetamine); repetitive behavior consequent to confined or restricted housing (e.g. laboratory caging); and repetitive behavior associated with specific inbred mouse strains. We have reviewed the literature from each of these categories of animal models, and discuss their multiple etiologies in light of a potential shared common pathophysiology: alterations in cortical-basal ganglia circuitry. Our own work with deer mice as a model of restricted, repetitive behavior suggests reduced activity in the indirect pathway of the basal ganglia, and has identified novel potential therapeutic targets. Other promising models are emerging that can take full advantage of modern genetics and molecular neuroscience that can be used to elucidate the pathophysiology of restricted, repetitive behavior. However, much more work must be done in this area to uncover the mechanisms underlying restricted, repetitive behavior, a critical step in finding effective new treatments for individuals with autism spectrum disorders. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-006 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] Modeling Restricted Repetitive Behavior in Animals [Texte imprimé et/ou numérique] / Allison BECHARD, Auteur ; Mark LEWIS, Auteur . - 8 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 8 p. Mots-clés : Repetitive behavior  Stereotypy  Cortical-basal ganglia circuitry  Autism spectrum disorders Index. décimale : PER Périodiques Résumé : Restricted, repetitive behavior is one of the three diagnostic domains for autism spectrum disorders, and commonly observed in a number of other neurodevelopmental disorders. Despite its clinical significance, effective treatments for restricted, repetitive behavior are limited including few, if any, pharmacological interventions with demonstrated efficacy. This is in large measure due to the lack of knowledge of the pathophysiological mechanisms that mediate the development and expression of repetitive behaviors in autism spectrum disorders. Therefore, animal models, particularly those that encompass both lower order and higher order repetitive behaviors, could be particularly useful. Such models could identify various potential etiologies, characterize commonalities in pathophysiology, identify novel potential therapeutic targets, and guide the development and validation of novel treatments. We have organized existing models of restricted, repetitive behavior in animals into four different categories: repetitive behavior resulting from a specific CNS insult (e.g. genetic mutation); repetitive behavior induced by specific pharmacological agents (e.g. amphetamine); repetitive behavior consequent to confined or restricted housing (e.g. laboratory caging); and repetitive behavior associated with specific inbred mouse strains. We have reviewed the literature from each of these categories of animal models, and discuss their multiple etiologies in light of a potential shared common pathophysiology: alterations in cortical-basal ganglia circuitry. Our own work with deer mice as a model of restricted, repetitive behavior suggests reduced activity in the indirect pathway of the basal ganglia, and has identified novel potential therapeutic targets. Other promising models are emerging that can take full advantage of modern genetics and molecular neuroscience that can be used to elucidate the pathophysiology of restricted, repetitive behavior. However, much more work must be done in this area to uncover the mechanisms underlying restricted, repetitive behavior, a critical step in finding effective new treatments for individuals with autism spectrum disorders. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-006 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

ASD-relevant Animal Models of the Foxp Family of Transcription Factors / J. Michael BOWERS in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 7 p. Titre : ASD-relevant Animal Models of the Foxp Family of Transcription Factors Type de document : Texte imprimé et/ou numérique Auteurs : J. Michael BOWERS, Auteur ; Genevieve KONOPKA, Auteur Article en page(s) : 7 p. Langues : Anglais (eng) Mots-clés : FOXP2  FOXP1  Autism  Genetics  Rodent vocalization Index. décimale : PER Périodiques Résumé : Autism is a neurodevelopmental disorder with a multifaceted association between genes and the environment. Currently, in the majority of patients, the etiology of autism is not known and coupled with increasing prevalence rates, along with the high degree of heritability of autism, the development of animal models is crucial for studying and developing therapies for autism. A key characteristic of autism is marked abnormalities in the acquisition and use of language. Thus, to understand and ultimately treat autism is an especially difficult task because no animal produces language, as it is defined in humans. In this review, we will discuss the FOXP family of genes, which are a group of transcription factors that have been linked to both autism, as well as language in humans. Due to the association of language/communication and the Foxp family of transcription factors, animal models with targeted disruptions of Foxp functioning are powerful tools for understanding the developmental signaling pathways that may be vulnerable in autism. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-010 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] ASD-relevant Animal Models of the Foxp Family of Transcription Factors [Texte imprimé et/ou numérique] / J. Michael BOWERS, Auteur ; Genevieve KONOPKA, Auteur . - 7 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 7 p. Mots-clés : FOXP2  FOXP1  Autism  Genetics  Rodent vocalization Index. décimale : PER Périodiques Résumé : Autism is a neurodevelopmental disorder with a multifaceted association between genes and the environment. Currently, in the majority of patients, the etiology of autism is not known and coupled with increasing prevalence rates, along with the high degree of heritability of autism, the development of animal models is crucial for studying and developing therapies for autism. A key characteristic of autism is marked abnormalities in the acquisition and use of language. Thus, to understand and ultimately treat autism is an especially difficult task because no animal produces language, as it is defined in humans. In this review, we will discuss the FOXP family of genes, which are a group of transcription factors that have been linked to both autism, as well as language in humans. Due to the association of language/communication and the Foxp family of transcription factors, animal models with targeted disruptions of Foxp functioning are powerful tools for understanding the developmental signaling pathways that may be vulnerable in autism. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-010 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

The BTBR T+tf/J (BTBR) Mouse Model of Autism / Kathryn K. CHADMAN in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 7 p. Titre : The BTBR T+tf/J (BTBR) Mouse Model of Autism Type de document : Texte imprimé et/ou numérique Auteurs : Kathryn K. CHADMAN, Auteur ; Sara R. GUARIGLIA, Auteur Article en page(s) : 7 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Mouse models of neuropsychiatric disorders are validated according to three different criteria: face validity, construct validity and predictive validity. Autism Spectrum Disorders (ASDs) are diagnosed behaviorally, therefore, mouse models of ASDs rely primarily on face validity. The three diagnostic criteria for ASDs are impairments in social interaction, communication and repetitive behavior, and/or restricted interests. The BTBR T+tf/J (BTBR) mice are an inbred strain used as model of ASDs. All three types of behavioral criteria have been evaluated in the BTBR mice. An advantage of using an inbred strain, such as BTBR is that, the mice are considered genetically identical and offer good controls for experimentation. The BTBR mice have demonstrated face validity for the three core behaviors that define ASDs. Low levels of social behavior, altered communication and spontaneous grooming comprise the behavioral phenotype of the BTBR mice. For construct validity, the BTBR mice have some physiological characteristics similar to humans with ASDs. Several drug and behavioral treatments for ASDs have been examined in the BTBR mice; however this area of research is still being developed. This review will offer a description of the behavior and physiology of the BTBR mice as a model for ASDs. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-009 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] The BTBR T+tf/J (BTBR) Mouse Model of Autism [Texte imprimé et/ou numérique] / Kathryn K. CHADMAN, Auteur ; Sara R. GUARIGLIA, Auteur . - 7 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 7 p. Index. décimale : PER Périodiques Résumé : Mouse models of neuropsychiatric disorders are validated according to three different criteria: face validity, construct validity and predictive validity. Autism Spectrum Disorders (ASDs) are diagnosed behaviorally, therefore, mouse models of ASDs rely primarily on face validity. The three diagnostic criteria for ASDs are impairments in social interaction, communication and repetitive behavior, and/or restricted interests. The BTBR T+tf/J (BTBR) mice are an inbred strain used as model of ASDs. All three types of behavioral criteria have been evaluated in the BTBR mice. An advantage of using an inbred strain, such as BTBR is that, the mice are considered genetically identical and offer good controls for experimentation. The BTBR mice have demonstrated face validity for the three core behaviors that define ASDs. Low levels of social behavior, altered communication and spontaneous grooming comprise the behavioral phenotype of the BTBR mice. For construct validity, the BTBR mice have some physiological characteristics similar to humans with ASDs. Several drug and behavioral treatments for ASDs have been examined in the BTBR mice; however this area of research is still being developed. This review will offer a description of the behavior and physiology of the BTBR mice as a model for ASDs. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-009 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

Magnetic Resonance Imaging as a Tool for the Study of Mouse Models of Autism / Jacob ELLEGOOD in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 8 p. Titre : Magnetic Resonance Imaging as a Tool for the Study of Mouse Models of Autism Type de document : Texte imprimé et/ou numérique Auteurs : Jacob ELLEGOOD, Auteur ; R. Mark HENKELMAN, Auteur ; Jason P. LERCH, Auteur Article en page(s) : 8 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism is a heterogeneous disorder, in both its behaviour and genetics. This heterogeneity has led to inconsistencies in the neuroanatomical findings in human autistic patients. The benefit of a model system, such as the mouse, is that there could be a decrease in the heterogeneity of the genetics and standardization of the environment could be done, in order to determine a specific anatomical phenotype, which is representative of a specific genotype. Magnetic Resonance Imaging (MRI) has been used quite extensively to examine morphological changes in the mouse brain; however, examining volume and tissue microstructure changes in mouse models of autism with MRI, is just in its infancy. This review will discuss the current research on anatomical phenotyping in mouse models of autism. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-008 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] Magnetic Resonance Imaging as a Tool for the Study of Mouse Models of Autism [Texte imprimé et/ou numérique] / Jacob ELLEGOOD, Auteur ; R. Mark HENKELMAN, Auteur ; Jason P. LERCH, Auteur . - 8 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 8 p. Index. décimale : PER Périodiques Résumé : Autism is a heterogeneous disorder, in both its behaviour and genetics. This heterogeneity has led to inconsistencies in the neuroanatomical findings in human autistic patients. The benefit of a model system, such as the mouse, is that there could be a decrease in the heterogeneity of the genetics and standardization of the environment could be done, in order to determine a specific anatomical phenotype, which is representative of a specific genotype. Magnetic Resonance Imaging (MRI) has been used quite extensively to examine morphological changes in the mouse brain; however, examining volume and tissue microstructure changes in mouse models of autism with MRI, is just in its infancy. This review will discuss the current research on anatomical phenotyping in mouse models of autism. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-008 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

Mouse Models of 22q11.2-Associated Autism Spectrum Disorder / Noboru HIROI in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 9 p. Titre : Mouse Models of 22q11.2-Associated Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Noboru HIROI, Auteur ; Takeshi HIRAMOTO, Auteur ; Kathryn M. HARPER, Auteur ; Go SUZUKI, Auteur ; Shuken BOKU, Auteur Article en page(s) : 9 p. Langues : Anglais (eng) Mots-clés : Tbx1  Sept5  22q11.2  Syndromic ASD  Copy number variation Index. décimale : PER Périodiques Résumé : Copy number variation (CNV) of human chromosome 22q11.2 is associated with an elevated rate of autism spectrum disorder (ASD) and represents one of syndromic ASDs with rare genetic variants. However, the precise genetic basis of this association remains unclear due to its relatively large hemizygous and duplication region, including more than 30 genes. Previous studies using genetic mouse models suggested that although not all 22q11.2 genes contribute to ASD symptomatology, more than one 22q11.2 genes have distinct phenotypic targets for ASD symptoms. Our data show that deficiency of the two 22q11.2 genes Tbx1 and Sept5 causes distinct phenotypic sets of ASD symptoms. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-001 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] Mouse Models of 22q11.2-Associated Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Noboru HIROI, Auteur ; Takeshi HIRAMOTO, Auteur ; Kathryn M. HARPER, Auteur ; Go SUZUKI, Auteur ; Shuken BOKU, Auteur . - 9 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 9 p. Mots-clés : Tbx1  Sept5  22q11.2  Syndromic ASD  Copy number variation Index. décimale : PER Périodiques Résumé : Copy number variation (CNV) of human chromosome 22q11.2 is associated with an elevated rate of autism spectrum disorder (ASD) and represents one of syndromic ASDs with rare genetic variants. However, the precise genetic basis of this association remains unclear due to its relatively large hemizygous and duplication region, including more than 30 genes. Previous studies using genetic mouse models suggested that although not all 22q11.2 genes contribute to ASD symptomatology, more than one 22q11.2 genes have distinct phenotypic targets for ASD symptoms. Our data show that deficiency of the two 22q11.2 genes Tbx1 and Sept5 causes distinct phenotypic sets of ASD symptoms. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-001 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

Immune Involvement in Autism Spectrum Disorder as a Basis for Animal Models / Elaine Y. HSIAO in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 6 p. Titre : Immune Involvement in Autism Spectrum Disorder as a Basis for Animal Models Type de document : Texte imprimé et/ou numérique Auteurs : Elaine Y. HSIAO, Auteur ; Paul H. PATTERSON, Auteur Article en page(s) : 6 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Several of the environmental stimuli suggested to play a role in the pathogenesis of ASD involve altered immune responses during gestation. In this review, we discuss maternal immune activation as a primary risk factor for ASD, with an emphasis on recent findings from animal models of prenatal immune challenges. We further address the presence of autoantibodies as an additional immune-related autism risk factor, drawing upon work done in rodent and monkey models. We then explore the intersection between genetic and environmental susceptibility, with a focus on gene-environment interactions and immune involvement, in genetic risk factors for autism. Finally, we provide emerging evidence for the role of immune dysregulation in the pathogenesis of ASD. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-003 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] Immune Involvement in Autism Spectrum Disorder as a Basis for Animal Models [Texte imprimé et/ou numérique] / Elaine Y. HSIAO, Auteur ; Paul H. PATTERSON, Auteur . - 6 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 6 p. Index. décimale : PER Périodiques Résumé : Several of the environmental stimuli suggested to play a role in the pathogenesis of ASD involve altered immune responses during gestation. In this review, we discuss maternal immune activation as a primary risk factor for ASD, with an emphasis on recent findings from animal models of prenatal immune challenges. We further address the presence of autoantibodies as an additional immune-related autism risk factor, drawing upon work done in rodent and monkey models. We then explore the intersection between genetic and environmental susceptibility, with a focus on gene-environment interactions and immune involvement, in genetic risk factors for autism. Finally, we provide emerging evidence for the role of immune dysregulation in the pathogenesis of ASD. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-003 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

Aripiprazole in patients with autistic spectrum disorders: a review and case reports / Eiji KIRINO in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 10 p. Titre : Aripiprazole in patients with autistic spectrum disorders: a review and case reports Type de document : Texte imprimé et/ou numérique Auteurs : Eiji KIRINO, Auteur Article en page(s) : 10 p. Langues : Anglais (eng) Mots-clés : Aripiprazole  Autistic spectrum disorder  Pervasive developmental disorders  Asperger’s disorder Index. décimale : PER Périodiques Résumé : Background: Although a significant amount of literature regarding use of aripiprazole (APZ) in autistic spectrum disorders (ASDs) has benne published, APZ is not approved for use in autism or ASDs in countries other than the United States. Even in the United States, approved use of APZ is limited to the patients with autism in children and adolescents. This review and case reports focus on the available evidence and clinical experience regarding the use of APZ in patients with ASDs including adults Methods: A literature review was conducted, using the PubMed search term ‘aripiprazole’ and(‘autistic spectrum disorder’, ‘pervasive developmental disorders’ or ‘Asperger’s disorder’).Results: In previous reports, APZ can target symptoms such as anxiety, depression, aggression, and irritability. Compared with other antipsychotics, APZ also causes fewer adverse events that can lead to drug discontinuation. The case reports supported the literature review: APZ has moderate sedative, antidepressant, and antianxiety effects, when used to treat ASDs. None of the patients experienced adverse reactions (e.g., extrapyramidal symptoms, weight gain, and sedation).Conclusion: APZ reduces aggression in ASDs and improves qualitative deficits in interpersonal interactions and motivation. APZ also causes fewer adverse events. APZ may be associated with favorable treatment compliance, and may improve treatment of ASDs. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-004 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] Aripiprazole in patients with autistic spectrum disorders: a review and case reports [Texte imprimé et/ou numérique] / Eiji KIRINO, Auteur . - 10 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 10 p. Mots-clés : Aripiprazole  Autistic spectrum disorder  Pervasive developmental disorders  Asperger’s disorder Index. décimale : PER Périodiques Résumé : Background: Although a significant amount of literature regarding use of aripiprazole (APZ) in autistic spectrum disorders (ASDs) has benne published, APZ is not approved for use in autism or ASDs in countries other than the United States. Even in the United States, approved use of APZ is limited to the patients with autism in children and adolescents. This review and case reports focus on the available evidence and clinical experience regarding the use of APZ in patients with ASDs including adults Methods: A literature review was conducted, using the PubMed search term ‘aripiprazole’ and(‘autistic spectrum disorder’, ‘pervasive developmental disorders’ or ‘Asperger’s disorder’).Results: In previous reports, APZ can target symptoms such as anxiety, depression, aggression, and irritability. Compared with other antipsychotics, APZ also causes fewer adverse events that can lead to drug discontinuation. The case reports supported the literature review: APZ has moderate sedative, antidepressant, and antianxiety effects, when used to treat ASDs. None of the patients experienced adverse reactions (e.g., extrapyramidal symptoms, weight gain, and sedation).Conclusion: APZ reduces aggression in ASDs and improves qualitative deficits in interpersonal interactions and motivation. APZ also causes fewer adverse events. APZ may be associated with favorable treatment compliance, and may improve treatment of ASDs. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-004 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

Beyond Widespread Mecp2 Deletions to Model Rett Syndrome: Conditional Spatio-Temporal Knockout, Single-Point Mutations and Transgenic Rescue Mice / Wei LI in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 7 p. Titre : Beyond Widespread Mecp2 Deletions to Model Rett Syndrome: Conditional Spatio-Temporal Knockout, Single-Point Mutations and Transgenic Rescue Mice Type de document : Texte imprimé et/ou numérique Auteurs : Wei LI, Auteur ; Lucas POZZO-MILLER, Auteur Article en page(s) : 7 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Rett syndrome (RTT) is one of the leading causes of intellectual disabilities in women. In addition to a few autistic features, characteristic symptoms that distinguish from classical autism include stereotypic hand movements, motor coordination deficits, breathing abnormalities, seizures and loss of acquired speech as well as purposeful hand use. RTT is highly associated with MECP2, the gene encoding for the transcription factor that binds methylated Cytosine in C-p-G islands in DNA, controlling gene expression and chromatin remodeling. In this review, we will briefly discuss current perspectives on MeCP2 function, and then will describe in detail novel mouse models of RTT based on loss-of-function of Mecp2 and their use for establishing rescue models, wherein we pay close attention to behavioral and morphological phenotypes. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-005 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] Beyond Widespread Mecp2 Deletions to Model Rett Syndrome: Conditional Spatio-Temporal Knockout, Single-Point Mutations and Transgenic Rescue Mice [Texte imprimé et/ou numérique] / Wei LI, Auteur ; Lucas POZZO-MILLER, Auteur . - 7 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 7 p. Index. décimale : PER Périodiques Résumé : Rett syndrome (RTT) is one of the leading causes of intellectual disabilities in women. In addition to a few autistic features, characteristic symptoms that distinguish from classical autism include stereotypic hand movements, motor coordination deficits, breathing abnormalities, seizures and loss of acquired speech as well as purposeful hand use. RTT is highly associated with MECP2, the gene encoding for the transcription factor that binds methylated Cytosine in C-p-G islands in DNA, controlling gene expression and chromatin remodeling. In this review, we will briefly discuss current perspectives on MeCP2 function, and then will describe in detail novel mouse models of RTT based on loss-of-function of Mecp2 and their use for establishing rescue models, wherein we pay close attention to behavioral and morphological phenotypes. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-005 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

Modeling Social Communication Deficits in Mouse Models of Autism / Caterina MICHETTI in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 7 p. Titre : Modeling Social Communication Deficits in Mouse Models of Autism Type de document : Texte imprimé et/ou numérique Auteurs : Caterina MICHETTI, Auteur ; Laura RICCERI, Auteur ; Maria Luisa SCATTONI, Auteur Article en page(s) : 7 p. Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Male and female mice emit ultrasonic vocalizations during infancy when pups are separated from mother and littermates, as well as at adulthood in different experimental/social contexts. Mouse ultrasonic vocalizations had become now a popular assay for behavioral phenotyping throughout the life-span of models of autism since this response represents the best option to detect deficits within the social communication domain in the mouse species. In the present review, we describe the available methods to elicit and record mouse ultrasonic vocalizations in different social contexts and at different ages. Behavioral data collected on autism animal models in these paradigms/contexts are also discussed. Moreover, we strongly emphasized the need of a standardization of the behavioral methods to better compare results from different laboratories. Thanks to the progresses of computer technology, researchers can now perform detailed analyses of the vocal repertoire (classifying ultrasonic vocalizations into different categories) in autism mouse models. Recently, these analyses have revealed unusual vocal patterns in selected mouse lines. This innovative approach allows to detect also qualitative alterations in the social communication repertoire usually not identified with the standard analysis of emission rate. Future studies should be aimed at performing quantitative and qualitative analyses of vocalization patterns also in preclinical studies evaluating potential treatments in validated autism mouse models. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-007 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] Modeling Social Communication Deficits in Mouse Models of Autism [Texte imprimé et/ou numérique] / Caterina MICHETTI, Auteur ; Laura RICCERI, Auteur ; Maria Luisa SCATTONI, Auteur . - 7 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 7 p. Index. décimale : PER Périodiques Résumé : Male and female mice emit ultrasonic vocalizations during infancy when pups are separated from mother and littermates, as well as at adulthood in different experimental/social contexts. Mouse ultrasonic vocalizations had become now a popular assay for behavioral phenotyping throughout the life-span of models of autism since this response represents the best option to detect deficits within the social communication domain in the mouse species. In the present review, we describe the available methods to elicit and record mouse ultrasonic vocalizations in different social contexts and at different ages. Behavioral data collected on autism animal models in these paradigms/contexts are also discussed. Moreover, we strongly emphasized the need of a standardization of the behavioral methods to better compare results from different laboratories. Thanks to the progresses of computer technology, researchers can now perform detailed analyses of the vocal repertoire (classifying ultrasonic vocalizations into different categories) in autism mouse models. Recently, these analyses have revealed unusual vocal patterns in selected mouse lines. This innovative approach allows to detect also qualitative alterations in the social communication repertoire usually not identified with the standard analysis of emission rate. Future studies should be aimed at performing quantitative and qualitative analyses of vocalization patterns also in preclinical studies evaluating potential treatments in validated autism mouse models. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-007 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409

Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to Autism / Jacob M. SMITH in Autism - Open Access, 2-S ([01/12/2012])  

Public ISBD [article]  inAutism - Open Access > 2-S [01/12/2012] . - 8 p. Titre : Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to Autism Type de document : Texte imprimé et/ou numérique Auteurs : Jacob M. SMITH, Auteur ; Elizabeth M. POWELL, Auteur Article en page(s) : 8 p. Langues : Anglais (eng) Mots-clés : HGF  MET  Interneuron  Forebrain  Attentional set-shifting  Reversal learning  Seizure  Plaur Index. décimale : PER Périodiques Résumé : Variants of MET, a receptor tyrosine kinase which binds the ligand Hepatocyte growth factor (HGF), have been linked to elevated risk for developing autism spectrum disorders (ASD) in humans. Though best known as a proto-oncogene, MET also plays important roles during normal development, including the development of the central nervous system. Recent studies in several mouse lines have shown that mice with reduced HGF-Met signaling have altered profiles of interneurons in the cortex, striatum, and hippocampus. Alterations in neuronal development, particularly in the cerebral cortex, may contribute to the pathology of developmental disorders, including autism. Other studies have shown changes in excitatory signaling in the Met-deficient cortex. Interestingly, mice with deficient Met signaling also show behavioral alterations characteristic of autism. Here we review anatomical and behavioral findings in mice with altered HGF - Met signaling. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-002 ER - Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409 [article] Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to Autism [Texte imprimé et/ou numérique] / Jacob M. SMITH, Auteur ; Elizabeth M. POWELL, Auteur . - 8 p. Langues : Anglais (eng) in Autism - Open Access > 2-S [01/12/2012] . - 8 p. Mots-clés : HGF  MET  Interneuron  Forebrain  Attentional set-shifting  Reversal learning  Seizure  Plaur Index. décimale : PER Périodiques Résumé : Variants of MET, a receptor tyrosine kinase which binds the ligand Hepatocyte growth factor (HGF), have been linked to elevated risk for developing autism spectrum disorders (ASD) in humans. Though best known as a proto-oncogene, MET also plays important roles during normal development, including the development of the central nervous system. Recent studies in several mouse lines have shown that mice with reduced HGF-Met signaling have altered profiles of interneurons in the cortex, striatum, and hippocampus. Alterations in neuronal development, particularly in the cerebral cortex, may contribute to the pathology of developmental disorders, including autism. Other studies have shown changes in excitatory signaling in the Met-deficient cortex. Interestingly, mice with deficient Met signaling also show behavioral alterations characteristic of autism. Here we review anatomical and behavioral findings in mice with altered HGF - Met signaling. En ligne : https://dx.doi.org/10.4172/2165-7890.S1-002 ER - Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=409