6 recherche sur le mot-clé 'sociability'

Early pyridoxine administration rescues autism-like behavior in the BTBR T+tf/J autistic model / Wenyu SHAO ; Yichun SU ; Jiayin LIU ; Jing LUO ; Yi LUO ; Lian WANG ; Xiaotang FAN in Research in Autism Spectrum Disorders, 115 (July 2024)  

Public ISBD [article]  inResearch in Autism Spectrum Disorders > 115 (July 2024) . - p.102410 Titre : Early pyridoxine administration rescues autism-like behavior in the BTBR T+tf/J autistic model Type de document : texte imprimé Auteurs : Wenyu SHAO, Auteur ; Yichun SU, Auteur ; Jiayin LIU, Auteur ; Jing LUO, Auteur ; Yi LUO, Auteur ; Lian WANG, Auteur ; Xiaotang FAN, Auteur Article en page(s) : p.102410 Langues : Anglais (eng) Mots-clés : Autism  Pyridoxine  Neuroinflammation  Oxidative stress  Sociability Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by social impairment and repetitive, stereotyped behaviors. An imbalanced oxidative stress status and neuroinflammation are involved in ASD development. In this study, we investigated the effects of pyridoxine, a form of vitamin B6 with potent anti-oxidant and anti-inflammatory features, on autism-like behavior in BTBR T + ltpr3tf/J (BTBR) mice, a model of autism. Mice received pyridoxine from postnatal days 7 to 14. Behavioral tests were conducted on 8-week-old male mice, and the inflammatory status and oxidative stress levels were also assessed in the mouse hippocampus. Postnatal pyridoxine treatment significantly improved social deficits, stereotyped behaviors, and cognitive deficits in BTBR mice. In addition, pyridoxine treatment alleviated neuroinflammation in the hippocampus manifested by reduced Iba1+ microglia and inflammatory factors, such as interleukin-1 (IL-1 ), IL-6, TNF-?, and NF-?B. Further, pyridoxine-treated BTBR mice had elevated Nrf2 and HO-1 in the hippocampus. Postnatal pyridoxine administration might improve autistic-like behaviors in BTBR mice via attenuating oxidative stress and neuroinflammation in the hippocampus. En ligne : https://doi.org/10.1016/j.rasd.2024.102410 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=532 [article] Early pyridoxine administration rescues autism-like behavior in the BTBR T+tf/J autistic model [texte imprimé] / Wenyu SHAO, Auteur ; Yichun SU, Auteur ; Jiayin LIU, Auteur ; Jing LUO, Auteur ; Yi LUO, Auteur ; Lian WANG, Auteur ; Xiaotang FAN, Auteur . - p.102410. Langues : Anglais (eng) in Research in Autism Spectrum Disorders > 115 (July 2024) . - p.102410 Mots-clés : Autism  Pyridoxine  Neuroinflammation  Oxidative stress  Sociability Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by social impairment and repetitive, stereotyped behaviors. An imbalanced oxidative stress status and neuroinflammation are involved in ASD development. In this study, we investigated the effects of pyridoxine, a form of vitamin B6 with potent anti-oxidant and anti-inflammatory features, on autism-like behavior in BTBR T + ltpr3tf/J (BTBR) mice, a model of autism. Mice received pyridoxine from postnatal days 7 to 14. Behavioral tests were conducted on 8-week-old male mice, and the inflammatory status and oxidative stress levels were also assessed in the mouse hippocampus. Postnatal pyridoxine treatment significantly improved social deficits, stereotyped behaviors, and cognitive deficits in BTBR mice. In addition, pyridoxine treatment alleviated neuroinflammation in the hippocampus manifested by reduced Iba1+ microglia and inflammatory factors, such as interleukin-1 (IL-1 ), IL-6, TNF-?, and NF-?B. Further, pyridoxine-treated BTBR mice had elevated Nrf2 and HO-1 in the hippocampus. Postnatal pyridoxine administration might improve autistic-like behaviors in BTBR mice via attenuating oxidative stress and neuroinflammation in the hippocampus. En ligne : https://doi.org/10.1016/j.rasd.2024.102410 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=532

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)  

Public ISBD [article]  inAutism Research > 4-6 (December 2011) . - p.393-400 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 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 [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] / 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)  

Public ISBD [article]  inMolecular Autism > 12 (2021) Titre : Major motor and gait deficits with sexual dimorphism in a Shank3 mutant mouse model Type de document : texte imprimé 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+/ΔC) and homozygote (Shank3 ΔC/ΔC)] 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 ΔC/ΔC 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 ΔC/ΔC were less affected by the mutation than males. Shank3+/ΔC mice showed impairments only in social novelty preference, grooming, and decreased mGluR5 expression and that were to a much lesser extent than in Shank3 ΔC/ΔC mice. LIMITATIONS: As Shank3 mutation is a haploinsufficiency, it is of interest to emphasize that Shank3+/ΔC mice showed only mild to no deficiencies compared to Shank3 ΔC/ΔC. 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 ΔC/ΔC mice show more pronounced alterations than Shank3+/ΔC. 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 [article] Major motor and gait deficits with sexual dimorphism in a Shank3 mutant mouse model [texte imprimé] / 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+/ΔC) and homozygote (Shank3 ΔC/ΔC)] 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 ΔC/ΔC 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 ΔC/ΔC were less affected by the mutation than males. Shank3+/ΔC mice showed impairments only in social novelty preference, grooming, and decreased mGluR5 expression and that were to a much lesser extent than in Shank3 ΔC/ΔC mice. LIMITATIONS: As Shank3 mutation is a haploinsufficiency, it is of interest to emphasize that Shank3+/ΔC mice showed only mild to no deficiencies compared to Shank3 ΔC/ΔC. 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 ΔC/ΔC mice show more pronounced alterations than Shank3+/ΔC. 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

Shank3 deficiency elicits autistic-like behaviors by activating p38? in hypothalamic AgRP neurons / Shanshan WU in Molecular Autism, 15 (2024)  

Public ISBD [article]  inMolecular Autism > 15 (2024) . - 14p. Titre : Shank3 deficiency elicits autistic-like behaviors by activating p38? in hypothalamic AgRP neurons Type de document : texte imprimé Auteurs : Shanshan WU, Auteur ; Jing WANG, Auteur ; Zicheng ZHANG, Auteur ; Xinchen JIN, Auteur ; Yang XU, Auteur ; Youwen SI, Auteur ; Yixiao LIANG, Auteur ; Yueping GE, Auteur ; Huidong ZHAN, Auteur ; Li PENG, Auteur ; Wenkai BI, Auteur ; Dandan LUO, Auteur ; Mengzhu LI, Auteur ; Bo MENG, Auteur ; Qingbo GUAN, Auteur ; Jiajun ZHAO, Auteur ; Ling GAO, Auteur ; Zhao HE, Auteur Article en page(s) : 14p. Langues : Anglais (eng) Mots-clés : Animals  Mice  Agouti-Related Protein/genetics/metabolism  Arcuate Nucleus of Hypothalamus/metabolism  Autistic Disorder/genetics/metabolism  Hypothalamus/metabolism  Microfilament Proteins/metabolism  Nerve Tissue Proteins/genetics/metabolism  Neurons/metabolism  Mitogen-Activated Protein Kinase 14/metabolism  AgRP  Autism  Shank3  Sociability  Stereotypic behavior  p38? Index. décimale : PER Périodiques Résumé : BACKGROUND: SH3 and multiple ankyrin repeat domains protein 3 (SHANK3) monogenic mutations or deficiency leads to excessive stereotypic behavior and impaired sociability, which frequently occur in autism cases. To date, the underlying mechanisms by which Shank3 mutation or deletion causes autism and the part of the brain in which Shank3 mutation leads to the autistic phenotypes are understudied. The hypothalamus is associated with stereotypic behavior and sociability. p38 , a mediator of inflammatory responses in the brain, has been postulated as a potential gene for certain cases of autism occurrence. However, it is unclear whether hypothalamus and p38 are involved in the development of autism caused by Shank3 mutations or deficiency. METHODS: Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and immunoblotting were used to assess alternated signaling pathways in the hypothalamus of Shank3 knockout (Shank3(-/-)) mice. Home-Cage real-time monitoring test was performed to record stereotypic behavior and three-chamber test was used to monitor the sociability of mice. Adeno-associated viruses 9 (AAV9) were used to express p38 in the arcuate nucleus (ARC) or agouti-related peptide (AgRP) neurons. D176A and F327S mutations expressed constitutively active p38 . T180A and Y182F mutations expressed inactive p38 . RESULTS: We found that Shank3 controls stereotypic behavior and sociability by regulating p38 activity in AgRP neurons. Phosphorylated p38 level in hypothalamus is significantly enhanced in Shank3(-/-) mice. Consistently, overexpression of p38 in ARC or AgRP neurons elicits excessive stereotypic behavior and impairs sociability in wild-type (WT) mice. Notably, activated p38 in AgRP neurons increases stereotypic behavior and impairs sociability. Conversely, inactivated p38 in AgRP neurons significantly ameliorates autistic behaviors of Shank3(-/-) mice. In contrast, activated p38 in pro-opiomelanocortin (POMC) neurons does not affect stereotypic behavior and sociability in mice. LIMITATIONS: We demonstrated that SHANK3 regulates the phosphorylated p38 level in the hypothalamus and inactivated p38 in AgRP neurons significantly ameliorates autistic behaviors of Shank3(-/-) mice. However, we did not clarify the biochemical mechanism of SHANK3 inhibiting p38 in AgRP neurons. CONCLUSIONS: These results demonstrate that the Shank3 deficiency caused autistic-like behaviors by activating p38 signaling in AgRP neurons, suggesting that p38 signaling in AgRP neurons is a potential therapeutic target for Shank3 mutant-related autism. En ligne : https://dx.doi.org/10.1186/s13229-024-00595-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538 [article] Shank3 deficiency elicits autistic-like behaviors by activating p38? in hypothalamic AgRP neurons [texte imprimé] / Shanshan WU, Auteur ; Jing WANG, Auteur ; Zicheng ZHANG, Auteur ; Xinchen JIN, Auteur ; Yang XU, Auteur ; Youwen SI, Auteur ; Yixiao LIANG, Auteur ; Yueping GE, Auteur ; Huidong ZHAN, Auteur ; Li PENG, Auteur ; Wenkai BI, Auteur ; Dandan LUO, Auteur ; Mengzhu LI, Auteur ; Bo MENG, Auteur ; Qingbo GUAN, Auteur ; Jiajun ZHAO, Auteur ; Ling GAO, Auteur ; Zhao HE, Auteur . - 14p. Langues : Anglais (eng) in Molecular Autism > 15 (2024) . - 14p. Mots-clés : Animals  Mice  Agouti-Related Protein/genetics/metabolism  Arcuate Nucleus of Hypothalamus/metabolism  Autistic Disorder/genetics/metabolism  Hypothalamus/metabolism  Microfilament Proteins/metabolism  Nerve Tissue Proteins/genetics/metabolism  Neurons/metabolism  Mitogen-Activated Protein Kinase 14/metabolism  AgRP  Autism  Shank3  Sociability  Stereotypic behavior  p38? Index. décimale : PER Périodiques Résumé : BACKGROUND: SH3 and multiple ankyrin repeat domains protein 3 (SHANK3) monogenic mutations or deficiency leads to excessive stereotypic behavior and impaired sociability, which frequently occur in autism cases. To date, the underlying mechanisms by which Shank3 mutation or deletion causes autism and the part of the brain in which Shank3 mutation leads to the autistic phenotypes are understudied. The hypothalamus is associated with stereotypic behavior and sociability. p38 , a mediator of inflammatory responses in the brain, has been postulated as a potential gene for certain cases of autism occurrence. However, it is unclear whether hypothalamus and p38 are involved in the development of autism caused by Shank3 mutations or deficiency. METHODS: Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway analysis and immunoblotting were used to assess alternated signaling pathways in the hypothalamus of Shank3 knockout (Shank3(-/-)) mice. Home-Cage real-time monitoring test was performed to record stereotypic behavior and three-chamber test was used to monitor the sociability of mice. Adeno-associated viruses 9 (AAV9) were used to express p38 in the arcuate nucleus (ARC) or agouti-related peptide (AgRP) neurons. D176A and F327S mutations expressed constitutively active p38 . T180A and Y182F mutations expressed inactive p38 . RESULTS: We found that Shank3 controls stereotypic behavior and sociability by regulating p38 activity in AgRP neurons. Phosphorylated p38 level in hypothalamus is significantly enhanced in Shank3(-/-) mice. Consistently, overexpression of p38 in ARC or AgRP neurons elicits excessive stereotypic behavior and impairs sociability in wild-type (WT) mice. Notably, activated p38 in AgRP neurons increases stereotypic behavior and impairs sociability. Conversely, inactivated p38 in AgRP neurons significantly ameliorates autistic behaviors of Shank3(-/-) mice. In contrast, activated p38 in pro-opiomelanocortin (POMC) neurons does not affect stereotypic behavior and sociability in mice. LIMITATIONS: We demonstrated that SHANK3 regulates the phosphorylated p38 level in the hypothalamus and inactivated p38 in AgRP neurons significantly ameliorates autistic behaviors of Shank3(-/-) mice. However, we did not clarify the biochemical mechanism of SHANK3 inhibiting p38 in AgRP neurons. CONCLUSIONS: These results demonstrate that the Shank3 deficiency caused autistic-like behaviors by activating p38 signaling in AgRP neurons, suggesting that p38 signaling in AgRP neurons is a potential therapeutic target for Shank3 mutant-related autism. En ligne : https://dx.doi.org/10.1186/s13229-024-00595-4 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=538

Sociability deficits after prenatal exposure to valproic acid are rescued by early social enrichment / Marcos CAMPOLONGO in Molecular Autism, 9 (2018)  

Public ISBD [article]  inMolecular Autism > 9 (2018) . - 36p. Titre : Sociability deficits after prenatal exposure to valproic acid are rescued by early social enrichment Type de document : texte imprimé Auteurs : Marcos CAMPOLONGO, Auteur ; Nadia KAZLAUSKAS, Auteur ; German FALASCO, Auteur ; Leandro URRUTIA, Auteur ; Natalí 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 [article] Sociability deficits after prenatal exposure to valproic acid are rescued by early social enrichment [texte imprimé] / Marcos CAMPOLONGO, Auteur ; Nadia KAZLAUSKAS, Auteur ; German FALASCO, Auteur ; Leandro URRUTIA, Auteur ; Natalí 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)  

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