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Sociability deficits after prenatal exposure to valproic acid are rescued by early social enrichment / M. CAMPOLONGO in Molecular Autism, 9 (2018)
[article]
Titre : Sociability deficits after prenatal exposure to valproic acid are rescued by early social enrichment Type de document : Texte imprimé et/ou numérique Auteurs : M. CAMPOLONGO, Auteur ; N. KAZLAUSKAS, Auteur ; G. FALASCO, Auteur ; L. URRUTIA, Auteur ; N. SALGUEIRO, Auteur ; C. HOCHT, Auteur ; Amaicha Mara DEPINO, Auteur Article en page(s) : 36p. Langues : Anglais (eng) Mots-clés : Animals Autism Spectrum Disorder/etiology/therapy Brain/diagnostic imaging Female Male Mice Pregnancy Prenatal Exposure Delayed Effects/drug therapy/etiology Social Behavior Socioenvironmental Therapy/methods Valproic Acid/administration & dosage/toxicity Autism spectrum disorder Dopamine Piriform cortex Sociability Index. décimale : PER Périodiques Résumé : Background: Autism spectrum disorder (ASD) is characterized by impaired social interactions and repetitive patterns of behavior. Symptoms appear in early life and persist throughout adulthood. Early social stimulation can help reverse some of the symptoms, but the biological mechanisms of these therapies are unknown. By analyzing the effects of early social stimulation on ASD-related behavior in the mouse, we aimed to identify brain structures that contribute to these behaviors. Methods: We injected pregnant mice with 600-mg/kg valproic acid (VPA) or saline (SAL) at gestational day 12.5 and evaluated the effect of weaning their offspring in cages containing only VPA animals, only SAL animals, or mixed. We analyzed juvenile play at PD21 and performed a battery of behavioral tests in adulthood. We then used preclinical PET imaging for an unbiased analysis of the whole brain of these mice and studied the function of the piriform cortex by c-Fos immunoreactivity and HPLC. Results: Compared to control animals, VPA-exposed animals play less as juveniles and exhibit a lower frequency of social interaction in adulthood when reared with other VPA mice. In addition, these animals were less likely to investigate social odors in the habituation/dishabituation olfactory test. However, when VPA animals were weaned with control animals, these behavioral alterations were not observed. Interestingly, repetitive behaviors and depression-related behaviors were not affected by social enrichment. We also found that VPA animals present high levels of glucose metabolism bilaterally in the piriform cortex (Pir), a region known to be involved in social behaviors. Moreover, we found alterations in the somatosensory, motor, and insular cortices. Remarkably, these effects were mostly reversed after social stimulation. To evaluate if changes in glucose metabolism in the Pir correlated with changes in neuronal activity, we measured c-Fos immunoreactivity in the Pir and found it increased in animals prenatally exposed to VPA. We further found increased dopamine turnover in the Pir. Both alterations were largely reversed by social enrichment. Conclusions: We show that early social enrichment can specifically rescue social deficits in a mouse model of ASD. Our results identified the Pir as a structure affected by VPA-exposure and social enrichment, suggesting that it could be a key component of the social brain circuitry. En ligne : https://dx.doi.org/10.1186/s13229-018-0221-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371
in Molecular Autism > 9 (2018) . - 36p.[article] Sociability deficits after prenatal exposure to valproic acid are rescued by early social enrichment [Texte imprimé et/ou numérique] / M. CAMPOLONGO, Auteur ; N. KAZLAUSKAS, Auteur ; G. FALASCO, Auteur ; L. URRUTIA, Auteur ; N. SALGUEIRO, Auteur ; C. HOCHT, Auteur ; Amaicha Mara DEPINO, Auteur . - 36p.
Langues : Anglais (eng)
in Molecular Autism > 9 (2018) . - 36p.
Mots-clés : Animals Autism Spectrum Disorder/etiology/therapy Brain/diagnostic imaging Female Male Mice Pregnancy Prenatal Exposure Delayed Effects/drug therapy/etiology Social Behavior Socioenvironmental Therapy/methods Valproic Acid/administration & dosage/toxicity Autism spectrum disorder Dopamine Piriform cortex Sociability Index. décimale : PER Périodiques Résumé : Background: Autism spectrum disorder (ASD) is characterized by impaired social interactions and repetitive patterns of behavior. Symptoms appear in early life and persist throughout adulthood. Early social stimulation can help reverse some of the symptoms, but the biological mechanisms of these therapies are unknown. By analyzing the effects of early social stimulation on ASD-related behavior in the mouse, we aimed to identify brain structures that contribute to these behaviors. Methods: We injected pregnant mice with 600-mg/kg valproic acid (VPA) or saline (SAL) at gestational day 12.5 and evaluated the effect of weaning their offspring in cages containing only VPA animals, only SAL animals, or mixed. We analyzed juvenile play at PD21 and performed a battery of behavioral tests in adulthood. We then used preclinical PET imaging for an unbiased analysis of the whole brain of these mice and studied the function of the piriform cortex by c-Fos immunoreactivity and HPLC. Results: Compared to control animals, VPA-exposed animals play less as juveniles and exhibit a lower frequency of social interaction in adulthood when reared with other VPA mice. In addition, these animals were less likely to investigate social odors in the habituation/dishabituation olfactory test. However, when VPA animals were weaned with control animals, these behavioral alterations were not observed. Interestingly, repetitive behaviors and depression-related behaviors were not affected by social enrichment. We also found that VPA animals present high levels of glucose metabolism bilaterally in the piriform cortex (Pir), a region known to be involved in social behaviors. Moreover, we found alterations in the somatosensory, motor, and insular cortices. Remarkably, these effects were mostly reversed after social stimulation. To evaluate if changes in glucose metabolism in the Pir correlated with changes in neuronal activity, we measured c-Fos immunoreactivity in the Pir and found it increased in animals prenatally exposed to VPA. We further found increased dopamine turnover in the Pir. Both alterations were largely reversed by social enrichment. Conclusions: We show that early social enrichment can specifically rescue social deficits in a mouse model of ASD. Our results identified the Pir as a structure affected by VPA-exposure and social enrichment, suggesting that it could be a key component of the social brain circuitry. En ligne : https://dx.doi.org/10.1186/s13229-018-0221-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=371 The sociability spectrum: evidence from reciprocal genetic copy number variations / Alejandro LÓPEZ-TOBÓN in Molecular Autism, 11 (2020)
[article]
Titre : The sociability spectrum: evidence from reciprocal genetic copy number variations Type de document : Texte imprimé et/ou numérique Auteurs : Alejandro LÓPEZ-TOBÓN, Auteur ; Sebastiano TRATTARO, Auteur ; Giuseppe TESTA, Auteur Article en page(s) : 50 p. Langues : Anglais (eng) Mots-clés : 7dupASD 7q11.23 Autism spectrum disorders Hypersociability Sociability William-Beuren syndrome iPSCs Index. décimale : PER Périodiques Résumé : Sociability entails some of the most complex behaviors processed by the central nervous system. It includes the detection, integration, and interpretation of social cues and elaboration of context-specific responses that are quintessentially species-specific. There is an ever-growing accumulation of molecular associations to autism spectrum disorders (ASD), from causative genes to endophenotypes across multiple functional layers; these however, have rarely been put in context with the opposite manifestation featured in hypersociability syndromes. Genetic copy number variations (CNVs) allow to investigate the relationships between gene dosage and its corresponding phenotypes. In particular, CNVs of the 7q11.23 locus, which manifest diametrically opposite social behaviors, offer a privileged window to look into the molecular substrates underlying the developmental trajectories of the social brain. As by definition sociability is studied in humans postnatally, the developmental fluctuations causing social impairments have thus far remained a black box. Here, we review key evidence of molecular players involved at both ends of the sociability spectrum, focusing on genetic and functional associations of neuroendocrine regulators and synaptic transmission pathways. We then proceed to propose the existence of a molecular axis centered around the paradigmatic dosage imbalances at the 7q11.23 locus, regulating networks responsible for the development of social behavior in humans and highlight the key role that neurodevelopmental models from reprogrammed pluripotent cells will play for its understanding. En ligne : http://dx.doi.org/10.1186/s13229-020-00347-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427
in Molecular Autism > 11 (2020) . - 50 p.[article] The sociability spectrum: evidence from reciprocal genetic copy number variations [Texte imprimé et/ou numérique] / Alejandro LÓPEZ-TOBÓN, Auteur ; Sebastiano TRATTARO, Auteur ; Giuseppe TESTA, Auteur . - 50 p.
Langues : Anglais (eng)
in Molecular Autism > 11 (2020) . - 50 p.
Mots-clés : 7dupASD 7q11.23 Autism spectrum disorders Hypersociability Sociability William-Beuren syndrome iPSCs Index. décimale : PER Périodiques Résumé : Sociability entails some of the most complex behaviors processed by the central nervous system. It includes the detection, integration, and interpretation of social cues and elaboration of context-specific responses that are quintessentially species-specific. There is an ever-growing accumulation of molecular associations to autism spectrum disorders (ASD), from causative genes to endophenotypes across multiple functional layers; these however, have rarely been put in context with the opposite manifestation featured in hypersociability syndromes. Genetic copy number variations (CNVs) allow to investigate the relationships between gene dosage and its corresponding phenotypes. In particular, CNVs of the 7q11.23 locus, which manifest diametrically opposite social behaviors, offer a privileged window to look into the molecular substrates underlying the developmental trajectories of the social brain. As by definition sociability is studied in humans postnatally, the developmental fluctuations causing social impairments have thus far remained a black box. Here, we review key evidence of molecular players involved at both ends of the sociability spectrum, focusing on genetic and functional associations of neuroendocrine regulators and synaptic transmission pathways. We then proceed to propose the existence of a molecular axis centered around the paradigmatic dosage imbalances at the 7q11.23 locus, regulating networks responsible for the development of social behavior in humans and highlight the key role that neurodevelopmental models from reprogrammed pluripotent cells will play for its understanding. En ligne : http://dx.doi.org/10.1186/s13229-020-00347-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=427 Genetically inbred Balb/c mice differ from outbred Swiss Webster mice on discrete measures of sociability: relevance to a genetic mouse model of autism spectrum disorders / Luis F. JACOME in Autism Research, 4-6 (December 2011)
[article]
Titre : Genetically inbred Balb/c mice differ from outbred Swiss Webster mice on discrete measures of sociability: relevance to a genetic mouse model of autism spectrum disorders Type de document : Texte imprimé et/ou numérique Auteurs : Luis F. JACOME, Auteur ; Jessica A. BURKET, Auteur ; Amy L. HERNDON, Auteur ; Stephen I. DEUTSCH, Auteur Année de publication : 2012 Article en page(s) : p.393-400 Langues : Anglais (eng) Mots-clés : Balb/c mouse strain sociability autism spectrum disorders Index. décimale : PER Périodiques Résumé : The Balb/c mouse is proposed as a model of human disorders with prominent deficits of sociability, such as autism spectrum disorders (ASDs) that may involve pathophysiological disruption of NMDA receptor-mediated neurotransmission. A standard procedure was used to measure sociability in 8-week-old male genetically inbred Balb/c and outbred Swiss Webster mice. Moreover, because impaired sociability may influence the social behavior of stimulus mice, we also measured the proportion of total episodes of social approach made by the stimulus mouse while test and stimulus mice were allowed to interact freely. Three raters with good inter-rater agreement evaluated operationally defined measures of sociability chosen because of their descriptive similarity to deficits of social behavior reported in persons with ASDs. The data support previous reports that the Balb/c mouse is a genetic mouse model of impaired sociability. The data also show that the behavior of the social stimulus mouse is influenced by the impaired sociability of the Balb/c strain. Interestingly, operationally defined measures of sociability did not necessarily correlate with each other within mouse strain and the profile of correlated measures differed between strains. Finally, “stereotypic” behaviors (i.e. rearing, grooming and wall climbing) recorded during the session of free interaction between the test and social stimulus mice were more intensely displayed by Swiss Webster than Balb/c mice, suggesting that the domains of sociability and “restricted repetitive and stereotyped patterns of behavior” are independent of each other in the Balb/c strain. En ligne : http://dx.doi.org/10.1002/aur.218 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=151
in Autism Research > 4-6 (December 2011) . - p.393-400[article] Genetically inbred Balb/c mice differ from outbred Swiss Webster mice on discrete measures of sociability: relevance to a genetic mouse model of autism spectrum disorders [Texte imprimé et/ou numérique] / Luis F. JACOME, Auteur ; Jessica A. BURKET, Auteur ; Amy L. HERNDON, Auteur ; Stephen I. DEUTSCH, Auteur . - 2012 . - p.393-400.
Langues : Anglais (eng)
in Autism Research > 4-6 (December 2011) . - p.393-400
Mots-clés : Balb/c mouse strain sociability autism spectrum disorders Index. décimale : PER Périodiques Résumé : The Balb/c mouse is proposed as a model of human disorders with prominent deficits of sociability, such as autism spectrum disorders (ASDs) that may involve pathophysiological disruption of NMDA receptor-mediated neurotransmission. A standard procedure was used to measure sociability in 8-week-old male genetically inbred Balb/c and outbred Swiss Webster mice. Moreover, because impaired sociability may influence the social behavior of stimulus mice, we also measured the proportion of total episodes of social approach made by the stimulus mouse while test and stimulus mice were allowed to interact freely. Three raters with good inter-rater agreement evaluated operationally defined measures of sociability chosen because of their descriptive similarity to deficits of social behavior reported in persons with ASDs. The data support previous reports that the Balb/c mouse is a genetic mouse model of impaired sociability. The data also show that the behavior of the social stimulus mouse is influenced by the impaired sociability of the Balb/c strain. Interestingly, operationally defined measures of sociability did not necessarily correlate with each other within mouse strain and the profile of correlated measures differed between strains. Finally, “stereotypic” behaviors (i.e. rearing, grooming and wall climbing) recorded during the session of free interaction between the test and social stimulus mice were more intensely displayed by Swiss Webster than Balb/c mice, suggesting that the domains of sociability and “restricted repetitive and stereotyped patterns of behavior” are independent of each other in the Balb/c strain. En ligne : http://dx.doi.org/10.1002/aur.218 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=151 Major motor and gait deficits with sexual dimorphism in a Shank3 mutant mouse model / Emmanuel MATAS in Molecular Autism, 12 (2021)
[article]
Titre : Major motor and gait deficits with sexual dimorphism in a Shank3 mutant mouse model Type de document : Texte imprimé et/ou numérique Auteurs : Emmanuel MATAS, Auteur ; Alexandre MAISTERRENA, Auteur ; Mathieu THABAULT, Auteur ; Eric BALADO, Auteur ; Maureen FRANCHETEAU, Auteur ; Anais BALBOUS, Auteur ; Laurie GALVAN, Auteur ; Mohamed JABER, Auteur Langues : Anglais (eng) Mots-clés : Cerebellum Crus I Crus II Gait Motor coordination Purkinje cells Sociability mGluR5 Index. décimale : PER Périodiques Résumé : BACKGROUND: Contrasting findings were reported in several animal models with a Shank3 mutation used to induce various autism spectrum disorder (ASD) symptoms. Here, we aimed at investigating behavioral, cellular, and molecular consequences of a C-terminal (frameshift in exon 21) deletion in Shank3 protein in mice, a mutation that is also found in clinical conditions and which results in loss of major isoforms of Shank3. A special focus was made on cerebellar related parameters. METHODS: All three genotypes were analyzed [wild type (WT), heterozygote (Shank3+/?C) and homozygote (Shank3 ?C/?C)] and males and females were separated into two distinct groups. Motor and social behavior, gait, Purkinje cells (PC) and glutamatergic protein levels were determined. Behavioral and cellular procedures used here were previously validated using two environmental animal models of ASD. ANOVA and post-hoc analysis were used for statistical analysis. RESULTS: Shank3 ?C/?C mice showed significant impairments in social novelty preference, stereotyped behavior and gait. These were accompanied by a decreased number of PC in restricted cerebellar sub-regions and decreased cerebellar expression of mGluR5. Females Shank3 ?C/?C were less affected by the mutation than males. Shank3+/?C mice showed impairments only in social novelty preference, grooming, and decreased mGluR5 expression and that were to a much lesser extent than in Shank3 ?C/?C mice. LIMITATIONS: As Shank3 mutation is a haploinsufficiency, it is of interest to emphasize that Shank3+/?C mice showed only mild to no deficiencies compared to Shank3 ?C/?C. CONCLUSIONS: Our findings indicate that several behavioral, cellular, and molecular parameters are affected in this animal model. The reported deficits are more pronounced in males than in females. Additionally, male Shank3 ?C/?C mice show more pronounced alterations than Shank3+/?C. Together with our previous findings in two environmental animal models of ASD, our studies indicate that gait dysfunction constitutes a robust set of motor ASD symptoms that may be considered for implementation in clinical settings as an early and quantitative diagnosis criteria. En ligne : http://dx.doi.org/10.1186/s13229-020-00412-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438
in Molecular Autism > 12 (2021)[article] Major motor and gait deficits with sexual dimorphism in a Shank3 mutant mouse model [Texte imprimé et/ou numérique] / Emmanuel MATAS, Auteur ; Alexandre MAISTERRENA, Auteur ; Mathieu THABAULT, Auteur ; Eric BALADO, Auteur ; Maureen FRANCHETEAU, Auteur ; Anais BALBOUS, Auteur ; Laurie GALVAN, Auteur ; Mohamed JABER, Auteur.
Langues : Anglais (eng)
in Molecular Autism > 12 (2021)
Mots-clés : Cerebellum Crus I Crus II Gait Motor coordination Purkinje cells Sociability mGluR5 Index. décimale : PER Périodiques Résumé : BACKGROUND: Contrasting findings were reported in several animal models with a Shank3 mutation used to induce various autism spectrum disorder (ASD) symptoms. Here, we aimed at investigating behavioral, cellular, and molecular consequences of a C-terminal (frameshift in exon 21) deletion in Shank3 protein in mice, a mutation that is also found in clinical conditions and which results in loss of major isoforms of Shank3. A special focus was made on cerebellar related parameters. METHODS: All three genotypes were analyzed [wild type (WT), heterozygote (Shank3+/?C) and homozygote (Shank3 ?C/?C)] and males and females were separated into two distinct groups. Motor and social behavior, gait, Purkinje cells (PC) and glutamatergic protein levels were determined. Behavioral and cellular procedures used here were previously validated using two environmental animal models of ASD. ANOVA and post-hoc analysis were used for statistical analysis. RESULTS: Shank3 ?C/?C mice showed significant impairments in social novelty preference, stereotyped behavior and gait. These were accompanied by a decreased number of PC in restricted cerebellar sub-regions and decreased cerebellar expression of mGluR5. Females Shank3 ?C/?C were less affected by the mutation than males. Shank3+/?C mice showed impairments only in social novelty preference, grooming, and decreased mGluR5 expression and that were to a much lesser extent than in Shank3 ?C/?C mice. LIMITATIONS: As Shank3 mutation is a haploinsufficiency, it is of interest to emphasize that Shank3+/?C mice showed only mild to no deficiencies compared to Shank3 ?C/?C. CONCLUSIONS: Our findings indicate that several behavioral, cellular, and molecular parameters are affected in this animal model. The reported deficits are more pronounced in males than in females. Additionally, male Shank3 ?C/?C mice show more pronounced alterations than Shank3+/?C. Together with our previous findings in two environmental animal models of ASD, our studies indicate that gait dysfunction constitutes a robust set of motor ASD symptoms that may be considered for implementation in clinical settings as an early and quantitative diagnosis criteria. En ligne : http://dx.doi.org/10.1186/s13229-020-00412-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=438