Behavioral Evaluation of Genetic Mouse Models of Autism / Mu YANG

Public ISBD in Autism Spectrum Disorders / David G. AMARAL Titre : Behavioral Evaluation of Genetic Mouse Models of Autism Type de document : texte imprimé Auteurs : Mu YANG, Auteur ; Maria Luisa SCATTONI, Auteur ; Kathryn K. CHADMAN, Auteur ; Jill L. SILVERMAN, Auteur ; Jacqueline N. CRAWLEY, Auteur Année de publication : 2011 Importance : p.906-934 Langues : Anglais (eng) Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=140 in Autism Spectrum Disorders / David G. AMARAL Behavioral Evaluation of Genetic Mouse Models of Autism [texte imprimé] / Mu YANG, Auteur ; Maria Luisa SCATTONI, Auteur ; Kathryn K. CHADMAN, Auteur ; Jill L. SILVERMAN, Auteur ; Jacqueline N. CRAWLEY, Auteur . - 2011 . - p.906-934. Langues : Anglais (eng) Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=140

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Contribution of the serotonergic system to developmental brain abnormalities in autism spectrum disorder / Kathryn K. CHADMAN ; Eric LONDON ; Thomas WISNIEWSKI ; Jerzy WEGIEL in Autism Research, 17-7 (July 2024)  

Public ISBD [article]  inAutism Research > 17-7 (July 2024) . - p.1300-1321 Titre : Contribution of the serotonergic system to developmental brain abnormalities in autism spectrum disorder Type de document : texte imprimé Auteurs : Kathryn K. CHADMAN, Auteur ; Eric LONDON, Auteur ; Thomas WISNIEWSKI, Auteur ; Jerzy WEGIEL, Auteur Article en page(s) : p.1300-1321 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Abstract This review highlights a key role of the serotonergic system in brain development and in distortions of normal brain development in early stages of fetal life resulting in cascades of abnormalities, including defects of neurogenesis, neuronal migration, neuronal growth, differentiation, and arborization, as well as defective neuronal circuit formation in the cortex, subcortical structures, brainstem, and cerebellum of autistic subjects. In autism, defects in regulation of neuronal growth are the most frequent and ubiquitous developmental changes associated with impaired neuron differentiation, smaller size, distorted shape, loss of spatial orientation, and distortion of cortex organization. Common developmental defects of the brain in autism include multiregional focal dysplastic changes contributing to local neuronal circuit distortion, epileptogenic activity, and epilepsy. There is a discrepancy between more than 500 reports demonstrating the contribution of the serotonergic system to autism's behavioral anomalies, highlighted by lack of studies of autistic subjects' brainstem raphe nuclei, the center of brain serotonergic innervation, and of the contribution of the serotonergic system to the diagnostic features of autism spectrum disorder (ASD). Discovery of severe fetal brainstem auditory system neuronal deficits and other anomalies leading to a spectrum of hearing deficits contributing to a cascade of behavioral alterations, including deficits of social and verbal communication in individuals with autism, is another argument to intensify postmortem studies of the type and topography of, and the severity of developmental defects in raphe nuclei and their contribution to abnormal brain development and to the broad spectrum of functional deficits and comorbid conditions in ASD. En ligne : https://dx.doi.org/https://doi.org/10.1002/aur.3123 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=533 [article] Contribution of the serotonergic system to developmental brain abnormalities in autism spectrum disorder [texte imprimé] / Kathryn K. CHADMAN, Auteur ; Eric LONDON, Auteur ; Thomas WISNIEWSKI, Auteur ; Jerzy WEGIEL, Auteur . - p.1300-1321. Langues : Anglais (eng) in Autism Research > 17-7 (July 2024) . - p.1300-1321 Index. décimale : PER Périodiques Résumé : Abstract This review highlights a key role of the serotonergic system in brain development and in distortions of normal brain development in early stages of fetal life resulting in cascades of abnormalities, including defects of neurogenesis, neuronal migration, neuronal growth, differentiation, and arborization, as well as defective neuronal circuit formation in the cortex, subcortical structures, brainstem, and cerebellum of autistic subjects. In autism, defects in regulation of neuronal growth are the most frequent and ubiquitous developmental changes associated with impaired neuron differentiation, smaller size, distorted shape, loss of spatial orientation, and distortion of cortex organization. Common developmental defects of the brain in autism include multiregional focal dysplastic changes contributing to local neuronal circuit distortion, epileptogenic activity, and epilepsy. There is a discrepancy between more than 500 reports demonstrating the contribution of the serotonergic system to autism's behavioral anomalies, highlighted by lack of studies of autistic subjects' brainstem raphe nuclei, the center of brain serotonergic innervation, and of the contribution of the serotonergic system to the diagnostic features of autism spectrum disorder (ASD). Discovery of severe fetal brainstem auditory system neuronal deficits and other anomalies leading to a spectrum of hearing deficits contributing to a cascade of behavioral alterations, including deficits of social and verbal communication in individuals with autism, is another argument to intensify postmortem studies of the type and topography of, and the severity of developmental defects in raphe nuclei and their contribution to abnormal brain development and to the broad spectrum of functional deficits and comorbid conditions in ASD. En ligne : https://dx.doi.org/https://doi.org/10.1002/aur.3123 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=533

Inbred strain preference in the BTBR T(+) Itpr3(tf) /J mouse model of autism spectrum disorder: Does the stranger mouse matter in social approach? / K. RYAN in Autism Research, 12-8 (August 2019)  

Public ISBD [article]  inAutism Research > 12-8 (August 2019) . - p.1184-1191 Titre : Inbred strain preference in the BTBR T(+) Itpr3(tf) /J mouse model of autism spectrum disorder: Does the stranger mouse matter in social approach? Type de document : texte imprimé Auteurs : K. RYAN, Auteur ; L. THOMPSON, Auteur ; P. A. MENDOZA, Auteur ; Kathryn K. CHADMAN, Auteur Article en page(s) : p.1184-1191 Langues : Anglais (eng) Mots-clés : Asd  Btbr  C57bl/6j  female  male  mice  social behavior  social preference Index. décimale : PER Périodiques Résumé : BTBR T(+) Itpr3(tf) /J (BTBR) mice have been used as a model of autism spectrum disorder (ASD) due to their low levels of sociability and high levels of repetitive grooming. These experiments explored social behavior in the BTBR and C57BL/6J mice using variations of the three-chambered social approach test. In the first test, the subject mice had a choice between a stranger mouse of the same strain or from a strain with a different level of sociability. The BTBR male mice demonstrated a strong preference for the more social C57BL/6J stranger mouse, as did the C57BL/6J male mice, although more moderately with sniff time only. The C57BL/6J female mice showed a moderate preference, sniff time only, for the BTBR stranger mouse, whereas the BTBR female mice did not show a preference. The second experiment examined whether the subject mouse preferred a stranger mouse or bedding from the stranger mouse home cage. Male BTBR mice always preferred bedding, whereas the C57BL/6J male mice did not show a preference. Both BTBR and C57BL/6J female mice preferred bedding when the stranger mouse was a different strain but not when the stranger mouse was the same strain. Therefore, the stranger mouse strain seems to influence the preference of the female mice more than the male mice. The mice preferred spending time in the chamber with the social smell but not the actual stranger mouse although not always significantly. This suggests that contact with a stranger mouse is more stressful or anxiety provoking than the smell. Autism Res 2019, 12: 1184-1191. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: BTBR T(+) Itpr3(tf) /J (BTBR) mice have been used as a model of autism spectrum disorder (ASD) due to their low levels of sociability and high levels of repetitive grooming. These experiments explored social behavior in the BTBR and C57BL/6J mice using variations of the three-chambered social approach test. These experiments examined how the sociability level of the stranger mouse affected the subject mouse's preference and if social odor was preferable to a social situation in the BTBR mice. The BTBR male mice demonstrated a strong preference for the more social C57BL/6J stranger mouse, as did the C57BL/6J male mice. The C57BL/6J female mice showed a moderate preference for the BTBR stranger mouse, whereas the BTBR female mice did not show a preference for either stranger mouse. The second modification let the subject mouse have a choice between a stranger mouse or bedding. Male BTBR mice preferred bedding, regardless of the strain of the stranger mouse, whereas the C57BL/6J male mice did not show a preference. Both BTBR and C57BL/6J female mice preferred bedding when the stranger mouse was a different strain but showed no preference when the stranger mouse was from the same strain. The stranger mouse strain seems to influence the female mice more. Male BTBR mice preferred spending time in the chamber with the social smell but not the actual mouse, suggesting that actual contact with a stranger mouse is more stressful or anxiety provoking. En ligne : http://dx.doi.org/10.1002/aur.2158 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=405 [article] Inbred strain preference in the BTBR T(+) Itpr3(tf) /J mouse model of autism spectrum disorder: Does the stranger mouse matter in social approach? [texte imprimé] / K. RYAN, Auteur ; L. THOMPSON, Auteur ; P. A. MENDOZA, Auteur ; Kathryn K. CHADMAN, Auteur . - p.1184-1191. Langues : Anglais (eng) in Autism Research > 12-8 (August 2019) . - p.1184-1191 Mots-clés : Asd  Btbr  C57bl/6j  female  male  mice  social behavior  social preference Index. décimale : PER Périodiques Résumé : BTBR T(+) Itpr3(tf) /J (BTBR) mice have been used as a model of autism spectrum disorder (ASD) due to their low levels of sociability and high levels of repetitive grooming. These experiments explored social behavior in the BTBR and C57BL/6J mice using variations of the three-chambered social approach test. In the first test, the subject mice had a choice between a stranger mouse of the same strain or from a strain with a different level of sociability. The BTBR male mice demonstrated a strong preference for the more social C57BL/6J stranger mouse, as did the C57BL/6J male mice, although more moderately with sniff time only. The C57BL/6J female mice showed a moderate preference, sniff time only, for the BTBR stranger mouse, whereas the BTBR female mice did not show a preference. The second experiment examined whether the subject mouse preferred a stranger mouse or bedding from the stranger mouse home cage. Male BTBR mice always preferred bedding, whereas the C57BL/6J male mice did not show a preference. Both BTBR and C57BL/6J female mice preferred bedding when the stranger mouse was a different strain but not when the stranger mouse was the same strain. Therefore, the stranger mouse strain seems to influence the preference of the female mice more than the male mice. The mice preferred spending time in the chamber with the social smell but not the actual stranger mouse although not always significantly. This suggests that contact with a stranger mouse is more stressful or anxiety provoking than the smell. Autism Res 2019, 12: 1184-1191. (c) 2019 International Society for Autism Research, Wiley Periodicals, Inc. LAY SUMMARY: BTBR T(+) Itpr3(tf) /J (BTBR) mice have been used as a model of autism spectrum disorder (ASD) due to their low levels of sociability and high levels of repetitive grooming. These experiments explored social behavior in the BTBR and C57BL/6J mice using variations of the three-chambered social approach test. These experiments examined how the sociability level of the stranger mouse affected the subject mouse's preference and if social odor was preferable to a social situation in the BTBR mice. The BTBR male mice demonstrated a strong preference for the more social C57BL/6J stranger mouse, as did the C57BL/6J male mice. The C57BL/6J female mice showed a moderate preference for the BTBR stranger mouse, whereas the BTBR female mice did not show a preference for either stranger mouse. The second modification let the subject mouse have a choice between a stranger mouse or bedding. Male BTBR mice preferred bedding, regardless of the strain of the stranger mouse, whereas the C57BL/6J male mice did not show a preference. Both BTBR and C57BL/6J female mice preferred bedding when the stranger mouse was a different strain but showed no preference when the stranger mouse was from the same strain. The stranger mouse strain seems to influence the female mice more. Male BTBR mice preferred spending time in the chamber with the social smell but not the actual mouse, suggesting that actual contact with a stranger mouse is more stressful or anxiety provoking. En ligne : http://dx.doi.org/10.1002/aur.2158 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=405

Minimal aberrant behavioral phenotypes of neuroligin-3 R451C knockin mice / Kathryn K. CHADMAN in Autism Research, 1-3 (June 2008)  

Public ISBD [article]  inAutism Research > 1-3 (June 2008) . - p.147-158 Titre : Minimal aberrant behavioral phenotypes of neuroligin-3 R451C knockin mice Type de document : texte imprimé Auteurs : Kathryn K. CHADMAN, Auteur ; Nathaniel HEINTZ, Auteur ; Shiaoching GONG, Auteur ; Maria Luisa SCATTONI, Auteur ; Sarah E. BOLTUCK, Auteur ; Shruti U. GANDHY, Auteur ; Jacqueline N. CRAWLEY, Auteur Année de publication : 2008 Article en page(s) : p.147-158 Langues : Anglais (eng) Mots-clés : autism mouse-model neuroligin behavior-phenotyping social-behavior Index. décimale : PER Périodiques Résumé : Neuroligin-3 is a member of the class of cell adhesion proteins that mediate synapse development and have been implicated in autism. Mice with the human R451C mutation (NL3), identical to the point mutation found in two brothers with autism spectrum disorders, were generated and phenotyped in multiple behavioral assays with face validity to the diagnostic symptoms of autism. No differences between NL3 and their wildtype (WT) littermate controls were detected on measures of juvenile reciprocal social interaction, adult social approach, cognitive abilities, and resistance to change in a spatial habit, findings which were replicated in several cohorts of males and females. Physical and procedural abilities were similar across genotypes on measures of general health, sensory abilities, sensorimotor gating, motor functions, and anxiety-related traits. Minor developmental differences were detected between NL3 and WT, including slightly different rates of somatic growth, slower righting reflexes at postnatal days 2-6, faster homing reflexes in females, and less vocalizations on postnatal day 8 in males. Significant differences in NL3 adults included somewhat longer latencies to fall from the rotarod, less vertical activity in the open field, and less acoustic startle to high decibel tones. The humanized R451C mutation in mice did not result in apparent autism-like phenotypes, but produced detectable functional consequences that may be interpreted in terms of physical development and/or reduced sensitivity to stimuli. En ligne : http://dx.doi.org/10.1002/aur.22 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931 [article] Minimal aberrant behavioral phenotypes of neuroligin-3 R451C knockin mice [texte imprimé] / Kathryn K. CHADMAN, Auteur ; Nathaniel HEINTZ, Auteur ; Shiaoching GONG, Auteur ; Maria Luisa SCATTONI, Auteur ; Sarah E. BOLTUCK, Auteur ; Shruti U. GANDHY, Auteur ; Jacqueline N. CRAWLEY, Auteur . - 2008 . - p.147-158. Langues : Anglais (eng) in Autism Research > 1-3 (June 2008) . - p.147-158 Mots-clés : autism mouse-model neuroligin behavior-phenotyping social-behavior Index. décimale : PER Périodiques Résumé : Neuroligin-3 is a member of the class of cell adhesion proteins that mediate synapse development and have been implicated in autism. Mice with the human R451C mutation (NL3), identical to the point mutation found in two brothers with autism spectrum disorders, were generated and phenotyped in multiple behavioral assays with face validity to the diagnostic symptoms of autism. No differences between NL3 and their wildtype (WT) littermate controls were detected on measures of juvenile reciprocal social interaction, adult social approach, cognitive abilities, and resistance to change in a spatial habit, findings which were replicated in several cohorts of males and females. Physical and procedural abilities were similar across genotypes on measures of general health, sensory abilities, sensorimotor gating, motor functions, and anxiety-related traits. Minor developmental differences were detected between NL3 and WT, including slightly different rates of somatic growth, slower righting reflexes at postnatal days 2-6, faster homing reflexes in females, and less vocalizations on postnatal day 8 in males. Significant differences in NL3 adults included somewhat longer latencies to fall from the rotarod, less vertical activity in the open field, and less acoustic startle to high decibel tones. The humanized R451C mutation in mice did not result in apparent autism-like phenotypes, but produced detectable functional consequences that may be interpreted in terms of physical development and/or reduced sensitivity to stimuli. En ligne : http://dx.doi.org/10.1002/aur.22 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=931

Pharmacological inhibition of the primary endocannabinoid producing enzyme, DGL-α, induces autism spectrum disorder-like and co-morbid phenotypes in adult C57BL/J mice / W. FYKE in Autism Research, 14-7 (July 2021)  

Public ISBD [article]  inAutism Research > 14-7 (July 2021) . - p.1375-1389 Titre : Pharmacological inhibition of the primary endocannabinoid producing enzyme, DGL-α, induces autism spectrum disorder-like and co-morbid phenotypes in adult C57BL/J mice Type de document : texte imprimé Auteurs : W. FYKE, Auteur ; J. M. ALARCON, Auteur ; M. VELINOV, Auteur ; Kathryn K. CHADMAN, Auteur Article en page(s) : p.1375-1389 Langues : Anglais (eng) Mots-clés : Animals  Anxiety  Autism Spectrum Disorder  Disease Models, Animal  Endocannabinoids  Male  Mice  Mice, Inbred C57BL  Phenotype  Dgl-?  autism spectrum disorders  mouse models  neurodevelopmental disorders Index. décimale : PER Périodiques Résumé : Accumulating evidence links dysfunction in the endocannabinoid system (ECS) with the pathology of neurodevelopmental disorders, particularly autism spectrum disorder (ASD). Variants in ECS genes CNR1 and DAGLA are associated with neurological phenotypes in humans. The endocannabinoids (eCBs), 2-AG and AEA, which act at the primary cannabinoid receptor (CB1), mediate behaviors relevant to neurodevelopmental disorders. The overlap between these eCBs is poorly understood. Most ECS studies have focused on stress responses, anxiety, and epilepsy, however, its role in social behavior and communication has only recently come under investigation. This represents a critical gap in our understanding of the ECS and its relationship to ASD. Furthermore, the increasing prevalence of ASD and a lack of therapeutics emphasize a crucial need for novel therapeutic targets. To this aim, we used an inhibitor of the eCB producing enzyme DGL-α, DO34, and the CB1 inverse agonist, rimonabant, to evaluate the role of the primary eCB, 2-AG, in ASD. Adult male C57BL/6J mice were used in a series of behavioral paradigms which assessed social behavior, social communication, repetitive behaviors, anxiety and locomotor activity. DO34 and rimonabant increased anxiety-like behavior, while only DO34 induced hyperactivity, social deficits, and repetitive self-grooming behavior. These data indicate that reduced 2-AG bioavailability, or CB1 inhibition, each induce unique respective behavioral phenotypes relevant to neurodevelopmental disorders, particularly ASD. This suggests fundamental differences in CB1 signaling via 2-AG and the CB1 receptor itself, particularly for social behaviors, and that 2-AG signaling may represent a target for the development of novel therapeutics. LAY SUMMARY: Endocannabinoids play a critical role in the developing nervous system. Alterations in the endocannabinoid system are linked to neurodevelopmental disorders. Studies suggest these variants may play a critical role in the core symptoms of autism spectrum disorder. In this study, pharmacological inhibition of the primary endocannabinoid producing enzyme, DGL-α, induced a constellation of deficits in behavioral domains associated with autism. En ligne : http://dx.doi.org/10.1002/aur.2520 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=449 [article] Pharmacological inhibition of the primary endocannabinoid producing enzyme, DGL-α, induces autism spectrum disorder-like and co-morbid phenotypes in adult C57BL/J mice [texte imprimé] / W. FYKE, Auteur ; J. M. ALARCON, Auteur ; M. VELINOV, Auteur ; Kathryn K. CHADMAN, Auteur . - p.1375-1389. Langues : Anglais (eng) in Autism Research > 14-7 (July 2021) . - p.1375-1389 Mots-clés : Animals  Anxiety  Autism Spectrum Disorder  Disease Models, Animal  Endocannabinoids  Male  Mice  Mice, Inbred C57BL  Phenotype  Dgl-?  autism spectrum disorders  mouse models  neurodevelopmental disorders Index. décimale : PER Périodiques Résumé : Accumulating evidence links dysfunction in the endocannabinoid system (ECS) with the pathology of neurodevelopmental disorders, particularly autism spectrum disorder (ASD). Variants in ECS genes CNR1 and DAGLA are associated with neurological phenotypes in humans. The endocannabinoids (eCBs), 2-AG and AEA, which act at the primary cannabinoid receptor (CB1), mediate behaviors relevant to neurodevelopmental disorders. The overlap between these eCBs is poorly understood. Most ECS studies have focused on stress responses, anxiety, and epilepsy, however, its role in social behavior and communication has only recently come under investigation. This represents a critical gap in our understanding of the ECS and its relationship to ASD. Furthermore, the increasing prevalence of ASD and a lack of therapeutics emphasize a crucial need for novel therapeutic targets. To this aim, we used an inhibitor of the eCB producing enzyme DGL-α, DO34, and the CB1 inverse agonist, rimonabant, to evaluate the role of the primary eCB, 2-AG, in ASD. Adult male C57BL/6J mice were used in a series of behavioral paradigms which assessed social behavior, social communication, repetitive behaviors, anxiety and locomotor activity. DO34 and rimonabant increased anxiety-like behavior, while only DO34 induced hyperactivity, social deficits, and repetitive self-grooming behavior. These data indicate that reduced 2-AG bioavailability, or CB1 inhibition, each induce unique respective behavioral phenotypes relevant to neurodevelopmental disorders, particularly ASD. This suggests fundamental differences in CB1 signaling via 2-AG and the CB1 receptor itself, particularly for social behaviors, and that 2-AG signaling may represent a target for the development of novel therapeutics. LAY SUMMARY: Endocannabinoids play a critical role in the developing nervous system. Alterations in the endocannabinoid system are linked to neurodevelopmental disorders. Studies suggest these variants may play a critical role in the core symptoms of autism spectrum disorder. In this study, pharmacological inhibition of the primary endocannabinoid producing enzyme, DGL-α, induced a constellation of deficits in behavioral domains associated with autism. En ligne : http://dx.doi.org/10.1002/aur.2520 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=449

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

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