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Brief Report: Feasibility of the Probabilistic Reversal Learning Task as an Outcome Measure in an Intervention Trial for Individuals with Autism Spectrum Disorder / Lauren M. SCHMITT in Journal of Autism and Developmental Disorders, 52-9 (September 2022)
[article]
Titre : Brief Report: Feasibility of the Probabilistic Reversal Learning Task as an Outcome Measure in an Intervention Trial for Individuals with Autism Spectrum Disorder Type de document : Texte imprimé et/ou numérique Auteurs : Lauren M. SCHMITT, Auteur ; John A. SWEENEY, Auteur ; Craig A. ERICKSON, Auteur ; Rebecca SHAFFER, Auteur Article en page(s) : p.4191-4199 Langues : Anglais (eng) Mots-clés : Autism Spectrum Disorder/psychology/therapy Feasibility Studies Humans Outcome Assessment, Health Care Reproducibility of Results Reversal Learning/physiology Autism spectrum disorder Cognitive flexibility Outcome measurement Reversal learning training (RS, LS). Index. décimale : PER Périodiques Résumé : Cognitive flexibility deficits are a hallmark feature of autism spectrum disorder (ASD), but few evidence-based behavioral interventions have successfully addressed this treatment target. Outcome measurement selection may help account for previous findings. The probabilistic reversal learning task (PRL) is a measure of cognitive flexibility previously validated for use in ASD, but its use as an outcome measure has not yet been assessed. The current study examined the feasibility, reproducibility, and sensitivity of PRL in a within-subjects trial of Regulating Together, a group-based intervention targeting emotion regulation. We demonstrated the PRL is highly feasible, showed test-retest reproducibility, and is sensitive to detect change following the intervention. Our findings demonstrate the PRL task may be a useful outcome measure of cognitive flexibility in future intervention trials in ASD. En ligne : http://dx.doi.org/10.1007/s10803-021-05288-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486
in Journal of Autism and Developmental Disorders > 52-9 (September 2022) . - p.4191-4199[article] Brief Report: Feasibility of the Probabilistic Reversal Learning Task as an Outcome Measure in an Intervention Trial for Individuals with Autism Spectrum Disorder [Texte imprimé et/ou numérique] / Lauren M. SCHMITT, Auteur ; John A. SWEENEY, Auteur ; Craig A. ERICKSON, Auteur ; Rebecca SHAFFER, Auteur . - p.4191-4199.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 52-9 (September 2022) . - p.4191-4199
Mots-clés : Autism Spectrum Disorder/psychology/therapy Feasibility Studies Humans Outcome Assessment, Health Care Reproducibility of Results Reversal Learning/physiology Autism spectrum disorder Cognitive flexibility Outcome measurement Reversal learning training (RS, LS). Index. décimale : PER Périodiques Résumé : Cognitive flexibility deficits are a hallmark feature of autism spectrum disorder (ASD), but few evidence-based behavioral interventions have successfully addressed this treatment target. Outcome measurement selection may help account for previous findings. The probabilistic reversal learning task (PRL) is a measure of cognitive flexibility previously validated for use in ASD, but its use as an outcome measure has not yet been assessed. The current study examined the feasibility, reproducibility, and sensitivity of PRL in a within-subjects trial of Regulating Together, a group-based intervention targeting emotion regulation. We demonstrated the PRL is highly feasible, showed test-retest reproducibility, and is sensitive to detect change following the intervention. Our findings demonstrate the PRL task may be a useful outcome measure of cognitive flexibility in future intervention trials in ASD. En ligne : http://dx.doi.org/10.1007/s10803-021-05288-y Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=486 Risperidone and the 5-HT2A Receptor Antagonist M100907 Improve Probabilistic Reversal Learning in BTBR T?+?tf/J Mice / Dionisio A. AMODEO in Autism Research, 7-5 (October 2014)
[article]
Titre : Risperidone and the 5-HT2A Receptor Antagonist M100907 Improve Probabilistic Reversal Learning in BTBR T?+?tf/J Mice Type de document : Texte imprimé et/ou numérique Auteurs : Dionisio A. AMODEO, Auteur ; Joshua H. JONES, Auteur ; John A. SWEENEY, Auteur ; Michael E. RAGOZZINO, Auteur Article en page(s) : p.555-567 Langues : Anglais (eng) Mots-clés : autism cognitive flexibility BTBR reversal learning serotonin risperidone Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interactions with restricted interests and repetitive behaviors (RRBs). RRBs can severely limit daily living and be particularly stressful to family members. To date, there are limited options for treating this feature in ASD. Risperidone, an atypical antipsychotic, is approved to treat irritability in ASD, but less is known about whether it is effective in treating “higher order” RRBs, for example cognitive inflexibility. Risperidone also has multiple receptor targets in which only a subset may be procognitive and others induce cognitive impairment. 5HT2A receptor blockade represents one promising and more targeted approach, as various preclinical studies have shown that 5HT2A receptor antagonists improve cognition. The present study investigated whether risperidone and/or M100907, a 5HT2A receptor antagonist, improved probabilistic reversal learning performance in the BTBR T?+?tf/J (BTBR) mouse model of autism. The effects of these treatments were also investigated in C57BL/6J (B6) mice as a comparison strain. Using a spatial reversal learning test with 80/20 probabilistic feedback, similar to one in which ASD individuals exhibit impairments, both risperidone (0.125?mg) and M100907 (0.01 and 0.1?mg) improved reversal learning in BTBR mice. Risperidone (0.125?mg) impaired reversal learning in B6 mice. Improvement in probabilistic reversal learning performance resulted from treatments enhancing the maintenance of the newly correct choice pattern. Because risperidone can lead to unwanted side effects, treatment with a specific 5HT2A receptor antagonist may improve cognitive flexibility in individuals with ASD while also minimizing unwanted side effects. Autism Res 2014, 7: 555–567. © 2014 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1395 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=241
in Autism Research > 7-5 (October 2014) . - p.555-567[article] Risperidone and the 5-HT2A Receptor Antagonist M100907 Improve Probabilistic Reversal Learning in BTBR T?+?tf/J Mice [Texte imprimé et/ou numérique] / Dionisio A. AMODEO, Auteur ; Joshua H. JONES, Auteur ; John A. SWEENEY, Auteur ; Michael E. RAGOZZINO, Auteur . - p.555-567.
Langues : Anglais (eng)
in Autism Research > 7-5 (October 2014) . - p.555-567
Mots-clés : autism cognitive flexibility BTBR reversal learning serotonin risperidone Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a neurodevelopmental disorder characterized by impaired social interactions with restricted interests and repetitive behaviors (RRBs). RRBs can severely limit daily living and be particularly stressful to family members. To date, there are limited options for treating this feature in ASD. Risperidone, an atypical antipsychotic, is approved to treat irritability in ASD, but less is known about whether it is effective in treating “higher order” RRBs, for example cognitive inflexibility. Risperidone also has multiple receptor targets in which only a subset may be procognitive and others induce cognitive impairment. 5HT2A receptor blockade represents one promising and more targeted approach, as various preclinical studies have shown that 5HT2A receptor antagonists improve cognition. The present study investigated whether risperidone and/or M100907, a 5HT2A receptor antagonist, improved probabilistic reversal learning performance in the BTBR T?+?tf/J (BTBR) mouse model of autism. The effects of these treatments were also investigated in C57BL/6J (B6) mice as a comparison strain. Using a spatial reversal learning test with 80/20 probabilistic feedback, similar to one in which ASD individuals exhibit impairments, both risperidone (0.125?mg) and M100907 (0.01 and 0.1?mg) improved reversal learning in BTBR mice. Risperidone (0.125?mg) impaired reversal learning in B6 mice. Improvement in probabilistic reversal learning performance resulted from treatments enhancing the maintenance of the newly correct choice pattern. Because risperidone can lead to unwanted side effects, treatment with a specific 5HT2A receptor antagonist may improve cognitive flexibility in individuals with ASD while also minimizing unwanted side effects. Autism Res 2014, 7: 555–567. © 2014 International Society for Autism Research, Wiley Periodicals, Inc. En ligne : http://dx.doi.org/10.1002/aur.1395 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=241 Altered medial prefrontal cortex and dorsal raphé activity predict genotype and correlate with abnormal learning behavior in a mouse model of autism-associated 2p16.3 deletion / Rebecca B. HUGHES in Autism Research, 15-4 (April 2022)
[article]
Titre : Altered medial prefrontal cortex and dorsal raphé activity predict genotype and correlate with abnormal learning behavior in a mouse model of autism-associated 2p16.3 deletion Type de document : Texte imprimé et/ou numérique Auteurs : Rebecca B. HUGHES, Auteur ; Jayde WHITTINGHAM-DOWD, Auteur ; Steven J. CLAPCOTE, Auteur ; Susan J. BROUGHTON, Auteur ; Neil DAWSON, Auteur Article en page(s) : p.614-627 Langues : Anglais (eng) Mots-clés : Animals Autism Spectrum Disorder/genetics Autistic Disorder Disease Models, Animal Dorsal Raphe Nucleus Genotype Humans Male Mice Prefrontal Cortex/diagnostic imaging Reversal Learning cognitive neuroscience copy number variation/copy number variants frontal lobe genotype-phenotype correlation imaging genetics mouse models serotonin Index. décimale : PER Périodiques Résumé : 2p16.3 deletion, involving NEUREXIN1 (NRXN1) heterozygous deletion, substantially increases the risk of developing autism and other neurodevelopmental disorders. We have a poor understanding of how NRXN1 heterozygosity impacts on brain function and cognition to increase the risk of developing the disorder. Here we characterize the impact of Nrxn1? heterozygosity on cerebral metabolism, in mice, using (14) C-2-deoxyglucose imaging. We also assess performance in an olfactory-based discrimination and reversal learning (OB-DaRL) task and locomotor activity. We use decision tree classifiers to test the predictive relationship between cerebral metabolism and Nrxn1? genotype. Our data show that Nrxn1? heterozygosity induces prefrontal cortex (medial prelimbic cortex, mPrL) hypometabolism and a contrasting dorsal raphé nucleus (DRN) hypermetabolism. Metabolism in these regions allows for the predictive classification of Nrxn1? genotype. Consistent with reduced mPrL glucose utilization, prefrontal cortex insulin receptor signaling is decreased in Nrxn1?(+/-) mice. Behaviorally, Nrxn1?(+/-) mice show enhanced learning of a novel discrimination, impaired reversal learning and an increased latency to make correct choices. In addition, male Nrxn1?(+/-) mice show hyperlocomotor activity. Correlative analysis suggests that mPrL hypometabolism contributes to the enhanced novel odor discrimination seen in Nrxn1?(+/-) mice, while DRN hypermetabolism contributes to their increased latency in making correct choices. The data show that Nrxn1? heterozygosity impacts on prefrontal cortex and serotonin system function, which contribute to the cognitive alterations seen in these animals. The data suggest that Nrxn1?(+/-) mice provide a translational model for the cognitive and behavioral alterations seen in autism and other neurodevelopmental disorders associated with 2p16.3 deletion. LAY SUMMARY: Deletion of the chromosomal region 2p16.3, involving reduced NEUREXIN1 gene expression, dramatically increases the risk of developing autism. Here, we show that reduced Neurexin1? expression, in mice, impacts on the prefrontal cortex and impairs cognitive flexibility. The data suggest that 2p16.3 deletion increases the risk of developing autism by impacting on the prefrontal cortex. Mice with the deletion are a useful model for testing new drugs to treat the cognitive flexibility problems experienced by people with autism. En ligne : https://dx.doi.org/10.1002/aur.2685 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473
in Autism Research > 15-4 (April 2022) . - p.614-627[article] Altered medial prefrontal cortex and dorsal raphé activity predict genotype and correlate with abnormal learning behavior in a mouse model of autism-associated 2p16.3 deletion [Texte imprimé et/ou numérique] / Rebecca B. HUGHES, Auteur ; Jayde WHITTINGHAM-DOWD, Auteur ; Steven J. CLAPCOTE, Auteur ; Susan J. BROUGHTON, Auteur ; Neil DAWSON, Auteur . - p.614-627.
Langues : Anglais (eng)
in Autism Research > 15-4 (April 2022) . - p.614-627
Mots-clés : Animals Autism Spectrum Disorder/genetics Autistic Disorder Disease Models, Animal Dorsal Raphe Nucleus Genotype Humans Male Mice Prefrontal Cortex/diagnostic imaging Reversal Learning cognitive neuroscience copy number variation/copy number variants frontal lobe genotype-phenotype correlation imaging genetics mouse models serotonin Index. décimale : PER Périodiques Résumé : 2p16.3 deletion, involving NEUREXIN1 (NRXN1) heterozygous deletion, substantially increases the risk of developing autism and other neurodevelopmental disorders. We have a poor understanding of how NRXN1 heterozygosity impacts on brain function and cognition to increase the risk of developing the disorder. Here we characterize the impact of Nrxn1? heterozygosity on cerebral metabolism, in mice, using (14) C-2-deoxyglucose imaging. We also assess performance in an olfactory-based discrimination and reversal learning (OB-DaRL) task and locomotor activity. We use decision tree classifiers to test the predictive relationship between cerebral metabolism and Nrxn1? genotype. Our data show that Nrxn1? heterozygosity induces prefrontal cortex (medial prelimbic cortex, mPrL) hypometabolism and a contrasting dorsal raphé nucleus (DRN) hypermetabolism. Metabolism in these regions allows for the predictive classification of Nrxn1? genotype. Consistent with reduced mPrL glucose utilization, prefrontal cortex insulin receptor signaling is decreased in Nrxn1?(+/-) mice. Behaviorally, Nrxn1?(+/-) mice show enhanced learning of a novel discrimination, impaired reversal learning and an increased latency to make correct choices. In addition, male Nrxn1?(+/-) mice show hyperlocomotor activity. Correlative analysis suggests that mPrL hypometabolism contributes to the enhanced novel odor discrimination seen in Nrxn1?(+/-) mice, while DRN hypermetabolism contributes to their increased latency in making correct choices. The data show that Nrxn1? heterozygosity impacts on prefrontal cortex and serotonin system function, which contribute to the cognitive alterations seen in these animals. The data suggest that Nrxn1?(+/-) mice provide a translational model for the cognitive and behavioral alterations seen in autism and other neurodevelopmental disorders associated with 2p16.3 deletion. LAY SUMMARY: Deletion of the chromosomal region 2p16.3, involving reduced NEUREXIN1 gene expression, dramatically increases the risk of developing autism. Here, we show that reduced Neurexin1? expression, in mice, impacts on the prefrontal cortex and impairs cognitive flexibility. The data suggest that 2p16.3 deletion increases the risk of developing autism by impacting on the prefrontal cortex. Mice with the deletion are a useful model for testing new drugs to treat the cognitive flexibility problems experienced by people with autism. En ligne : https://dx.doi.org/10.1002/aur.2685 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=473 Enhanced fear limits behavioral flexibility in Shank2-deficient mice / Miru YUN in Molecular Autism, 13 (2022)
[article]
Titre : Enhanced fear limits behavioral flexibility in Shank2-deficient mice Type de document : Texte imprimé et/ou numérique Auteurs : Miru YUN, Auteur ; Eunjoon KIM, Auteur ; Min Whan JUNG, Auteur Article en page(s) : 40 p. Langues : Anglais (eng) Mots-clés : Animals Autism Spectrum Disorder/genetics/psychology Conditioning, Classical Disease Models, Animal Fear Male Mice Mice, Knockout Nerve Tissue Proteins/genetics Water Classical conditioning Reversal learning Shank2 Index. décimale : PER Périodiques Résumé : BACKGROUND: A core symptom of autism spectrum disorder (ASD) is repetitive and restrictive patterns of behavior. Cognitive inflexibility has been proposed as a potential basis for these symptoms of ASD. More generally, behavioral inflexibility has been proposed to underlie repetitive and restrictive behavior in ASD. Here, we investigated whether and how behavioral flexibility is compromised in a widely used animal model of ASD. METHODS: We compared the behavioral performance of Shank2-knockout mice and wild-type littermates in reversal learning employing a probabilistic classical trace conditioning paradigm. A conditioned stimulus (odor) was paired with an unconditioned appetitive (water, 6Â Âul) or aversive (air puff) stimulus in a probabilistic manner. We also compared air puff-induced eye closure responses of Shank2-knockout and wild-type mice. RESULTS: Male, but not female, Shank2-knockout mice showed impaired reversal learning when the expected outcomes consisted of a water reward and a strong air puff. Moreover, male, but not female, Shank2-knockout mice showed stronger anticipatory eye closure responses to the air puff compared to wild-type littermates, raising the possibility that the impairment might reflect enhanced fear. In support of this contention, male Shank2-knockout mice showed intact reversal learning when the strong air puff was replaced with a mild air puff and when the expected outcomes consisted of only rewards. LIMITATIONS: We examined behavioral flexibility in one behavioral task (reversal learning in a probabilistic classical trace conditioning paradigm) using one ASD mouse model (Shank2-knockout mice). Thus, future work is needed to clarify the extent to which our findings (that enhanced fear limits behavioral flexibility in ASD) can explain the behavioral inflexibility associated with ASD. Also, we examined only the relationship between fear and behavioral flexibility, leaving open the question of whether abnormalities in processes other than fear contribute to behavioral inflexibility in ASD. Finally, the neurobiological mechanisms linking Shank2-knockout and enhanced fear remain to be elucidated. CONCLUSIONS: Our results indicate that enhanced fear suppresses reversal learning in the presence of an intact capability to learn cue-outcome contingency changes in Shank2-knockout mice. Our findings suggest that behavioral flexibility might be seriously limited by abnormal emotional responses in ASD. En ligne : http://dx.doi.org/10.1186/s13229-022-00518-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=491
in Molecular Autism > 13 (2022) . - 40 p.[article] Enhanced fear limits behavioral flexibility in Shank2-deficient mice [Texte imprimé et/ou numérique] / Miru YUN, Auteur ; Eunjoon KIM, Auteur ; Min Whan JUNG, Auteur . - 40 p.
Langues : Anglais (eng)
in Molecular Autism > 13 (2022) . - 40 p.
Mots-clés : Animals Autism Spectrum Disorder/genetics/psychology Conditioning, Classical Disease Models, Animal Fear Male Mice Mice, Knockout Nerve Tissue Proteins/genetics Water Classical conditioning Reversal learning Shank2 Index. décimale : PER Périodiques Résumé : BACKGROUND: A core symptom of autism spectrum disorder (ASD) is repetitive and restrictive patterns of behavior. Cognitive inflexibility has been proposed as a potential basis for these symptoms of ASD. More generally, behavioral inflexibility has been proposed to underlie repetitive and restrictive behavior in ASD. Here, we investigated whether and how behavioral flexibility is compromised in a widely used animal model of ASD. METHODS: We compared the behavioral performance of Shank2-knockout mice and wild-type littermates in reversal learning employing a probabilistic classical trace conditioning paradigm. A conditioned stimulus (odor) was paired with an unconditioned appetitive (water, 6Â Âul) or aversive (air puff) stimulus in a probabilistic manner. We also compared air puff-induced eye closure responses of Shank2-knockout and wild-type mice. RESULTS: Male, but not female, Shank2-knockout mice showed impaired reversal learning when the expected outcomes consisted of a water reward and a strong air puff. Moreover, male, but not female, Shank2-knockout mice showed stronger anticipatory eye closure responses to the air puff compared to wild-type littermates, raising the possibility that the impairment might reflect enhanced fear. In support of this contention, male Shank2-knockout mice showed intact reversal learning when the strong air puff was replaced with a mild air puff and when the expected outcomes consisted of only rewards. LIMITATIONS: We examined behavioral flexibility in one behavioral task (reversal learning in a probabilistic classical trace conditioning paradigm) using one ASD mouse model (Shank2-knockout mice). Thus, future work is needed to clarify the extent to which our findings (that enhanced fear limits behavioral flexibility in ASD) can explain the behavioral inflexibility associated with ASD. Also, we examined only the relationship between fear and behavioral flexibility, leaving open the question of whether abnormalities in processes other than fear contribute to behavioral inflexibility in ASD. Finally, the neurobiological mechanisms linking Shank2-knockout and enhanced fear remain to be elucidated. CONCLUSIONS: Our results indicate that enhanced fear suppresses reversal learning in the presence of an intact capability to learn cue-outcome contingency changes in Shank2-knockout mice. Our findings suggest that behavioral flexibility might be seriously limited by abnormal emotional responses in ASD. En ligne : http://dx.doi.org/10.1186/s13229-022-00518-1 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=491 Limited impact of Cntn4 mutation on autism-related traits in developing and adult C57BL/6J mice / R. T. MOLENHUIS in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
[article]
Titre : Limited impact of Cntn4 mutation on autism-related traits in developing and adult C57BL/6J mice Type de document : Texte imprimé et/ou numérique Auteurs : R. T. MOLENHUIS, Auteur ; Hilgo BRUINING, Auteur ; E. REMMELINK, Auteur ; L. DE VISSER, Auteur ; M. LOOS, Auteur ; J. P. H. BURBACH, Auteur ; M. J. KAS, Auteur Article en page(s) : p.6 Langues : Anglais (eng) Mots-clés : 3p deletion syndrome Autism spectrum disorder Behavior Cntn4 Developmental trajectories Hyperreactivity Mouse model Negative findings Reversal learning Schizophrenia Index. décimale : PER Périodiques Résumé : BACKGROUND: Mouse models offer an essential tool to unravel the impact of genetic mutations on autism-related phenotypes. The behavioral impact of some important candidate gene models for autism spectrum disorder (ASD) has not yet been studied, and existing characterizations mostly describe behavioral phenotypes at adult ages, disregarding the developmental nature of the disorder. In this context, the behavioral influence of CNTN4, one of the strongest suggested ASD candidate genes, is unknown. Here, we used our recently established developmental test battery to characterize the consequences of disruption of contactin 4 (Cntn4) on neurological, sensory, cognitive, and behavioral phenotypes across different developmental stages. METHODS: C57BL/6J mice with heterozygous and homozygous disruption of Cntn4 were studied through an extensive, partially longitudinal, test battery at various developmental stages, including various paradigms testing social and restricted repetitive behaviors. RESULTS: Developmental neurological and cognitive screenings revealed no significant differences between genotypes, and ASD-related behavioral domains were also unchanged in Cntn4-deficient versus wild-type mice. The impact of Cntn4-deficiency was found to be limited to increased startle responsiveness following auditory stimuli of different high amplitudes in heterozygous and homozygous Cntn4-deficient mice and enhanced acquisition in a spatial learning task in homozygous mice. CONCLUSIONS: Disruption of Cntn4 in the C57BL/6J background does not affect specific autism-related phenotypes in developing or adult mice but causes subtle non-disorder specific changes in sensory behavioral responses and cognitive performance. En ligne : http://dx.doi.org/10.1186/s11689-016-9140-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.6[article] Limited impact of Cntn4 mutation on autism-related traits in developing and adult C57BL/6J mice [Texte imprimé et/ou numérique] / R. T. MOLENHUIS, Auteur ; Hilgo BRUINING, Auteur ; E. REMMELINK, Auteur ; L. DE VISSER, Auteur ; M. LOOS, Auteur ; J. P. H. BURBACH, Auteur ; M. J. KAS, Auteur . - p.6.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.6
Mots-clés : 3p deletion syndrome Autism spectrum disorder Behavior Cntn4 Developmental trajectories Hyperreactivity Mouse model Negative findings Reversal learning Schizophrenia Index. décimale : PER Périodiques Résumé : BACKGROUND: Mouse models offer an essential tool to unravel the impact of genetic mutations on autism-related phenotypes. The behavioral impact of some important candidate gene models for autism spectrum disorder (ASD) has not yet been studied, and existing characterizations mostly describe behavioral phenotypes at adult ages, disregarding the developmental nature of the disorder. In this context, the behavioral influence of CNTN4, one of the strongest suggested ASD candidate genes, is unknown. Here, we used our recently established developmental test battery to characterize the consequences of disruption of contactin 4 (Cntn4) on neurological, sensory, cognitive, and behavioral phenotypes across different developmental stages. METHODS: C57BL/6J mice with heterozygous and homozygous disruption of Cntn4 were studied through an extensive, partially longitudinal, test battery at various developmental stages, including various paradigms testing social and restricted repetitive behaviors. RESULTS: Developmental neurological and cognitive screenings revealed no significant differences between genotypes, and ASD-related behavioral domains were also unchanged in Cntn4-deficient versus wild-type mice. The impact of Cntn4-deficiency was found to be limited to increased startle responsiveness following auditory stimuli of different high amplitudes in heterozygous and homozygous Cntn4-deficient mice and enhanced acquisition in a spatial learning task in homozygous mice. CONCLUSIONS: Disruption of Cntn4 in the C57BL/6J background does not affect specific autism-related phenotypes in developing or adult mice but causes subtle non-disorder specific changes in sensory behavioral responses and cognitive performance. En ligne : http://dx.doi.org/10.1186/s11689-016-9140-2 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348 Mice with Impaired Met Tyrosine Kinase Signaling Demonstrate Characteristics Relevant to Autism / Jacob M. SMITH in Autism - Open Access, 2-S ([01/12/2012])
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