Parental rearing and personality traits as predictors for adolescents with obsessive?compulsive disorder (OCD) / Yafeng ZHANG in Development and Psychopathology, 34-1 (February 2022)  

Public ISBD [article]  inDevelopment and Psychopathology > 34-1 (February 2022) . - p.387-394 Titre : Parental rearing and personality traits as predictors for adolescents with obsessive?compulsive disorder (OCD) Type de document : Texte imprimé et/ou numérique Auteurs : Yafeng ZHANG, Auteur ; Wei TIAN, Auteur ; Chao WANG, Auteur ; Bin GUO, Auteur ; Guangcan YAN, Auteur ; Hui YIN, Auteur ; Zuoming ZHANG, Auteur ; Yuchun TAO, Auteur ; Yixin LIU, Auteur ; Quan ZHOU, Auteur ; Limin WANG, Auteur Article en page(s) : p.387-394 Langues : Anglais (eng) Mots-clés : obsessive?compulsive disorder  parental rearing  personality traits  quantile regression  structural equation model Index. décimale : PER Périodiques Résumé : We aim to determine the correlation between parental rearing, personality traits, and obsessive?compulsive disorder (OCD) in different quantiles. In particular, we created an intermediary effect model in which parental rearing affects OCD through personality traits. All predictors were measured at the time of the survey, comprising parental rearing (paternal rearing and maternal rearing), demographics (grade and gender), and personality traits (neuroticism, extroversion, and psychoticism). These results suggest that (a) paternal emotional warmth was negatively correlated with OCD at the 0.40?0.80 quantile, while maternal emotional warmth was positively correlated with the OCD at the 0.45?0.69 quantile. (b) The correlation between negative parental rearing and OCD ranged from the 0.67 to 0.95 quantile for paternal punishment, 0.14?0.82 quantile for paternal overprotection, 0.05?0.36 and >0.50 quantile for maternal over-intervention and overprotection, and 0.08?0.88 quantile for maternal rejection. (c) Extroversion, neuroticism, and psychoticism were not only associated with OCD in a particular quantile but also mediated between parental rearing (namely parental emotional warmth, paternal punishment, paternal overprotection, maternal rejection, maternal over-intervention, and overprotection) and OCD. These findings provide targets for early interventions of OCD to improve the form of family education and personality traits and warrant validation. En ligne : http://dx.doi.org/10.1017/s095457942000108x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474 [article] Parental rearing and personality traits as predictors for adolescents with obsessive?compulsive disorder (OCD) [Texte imprimé et/ou numérique] / Yafeng ZHANG, Auteur ; Wei TIAN, Auteur ; Chao WANG, Auteur ; Bin GUO, Auteur ; Guangcan YAN, Auteur ; Hui YIN, Auteur ; Zuoming ZHANG, Auteur ; Yuchun TAO, Auteur ; Yixin LIU, Auteur ; Quan ZHOU, Auteur ; Limin WANG, Auteur . - p.387-394. Langues : Anglais (eng) in Development and Psychopathology > 34-1 (February 2022) . - p.387-394 Mots-clés : obsessive?compulsive disorder  parental rearing  personality traits  quantile regression  structural equation model Index. décimale : PER Périodiques Résumé : We aim to determine the correlation between parental rearing, personality traits, and obsessive?compulsive disorder (OCD) in different quantiles. In particular, we created an intermediary effect model in which parental rearing affects OCD through personality traits. All predictors were measured at the time of the survey, comprising parental rearing (paternal rearing and maternal rearing), demographics (grade and gender), and personality traits (neuroticism, extroversion, and psychoticism). These results suggest that (a) paternal emotional warmth was negatively correlated with OCD at the 0.40?0.80 quantile, while maternal emotional warmth was positively correlated with the OCD at the 0.45?0.69 quantile. (b) The correlation between negative parental rearing and OCD ranged from the 0.67 to 0.95 quantile for paternal punishment, 0.14?0.82 quantile for paternal overprotection, 0.05?0.36 and >0.50 quantile for maternal over-intervention and overprotection, and 0.08?0.88 quantile for maternal rejection. (c) Extroversion, neuroticism, and psychoticism were not only associated with OCD in a particular quantile but also mediated between parental rearing (namely parental emotional warmth, paternal punishment, paternal overprotection, maternal rejection, maternal over-intervention, and overprotection) and OCD. These findings provide targets for early interventions of OCD to improve the form of family education and personality traits and warrant validation. En ligne : http://dx.doi.org/10.1017/s095457942000108x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=474

Somatostatin-expressing interneurons of prefrontal cortex modulate social deficits in the Magel2 mouse model of autism / Mengyuan CHEN ; Daoqi MEI ; Shengli SHI ; Jisheng GUO ; Chao GAO ; Qi WANG ; Shuai ZHAO ; Xingxue YAN ; Huichun ZHANG ; Yanli WANG ; Bin GUO ; Yaodong ZHANG in Molecular Autism, 16 (2025)  

Public ISBD [article]  inMolecular Autism > 16 (2025) . - 18 Titre : Somatostatin-expressing interneurons of prefrontal cortex modulate social deficits in the Magel2 mouse model of autism Type de document : Texte imprimé et/ou numérique Auteurs : Mengyuan CHEN, Auteur ; Daoqi MEI, Auteur ; Shengli SHI, Auteur ; Jisheng GUO, Auteur ; Chao GAO, Auteur ; Qi WANG, Auteur ; Shuai ZHAO, Auteur ; Xingxue YAN, Auteur ; Huichun ZHANG, Auteur ; Yanli WANG, Auteur ; Bin GUO, Auteur ; Yaodong ZHANG, Auteur Article en page(s) : 18 Langues : Anglais (eng) Mots-clés : Animals  Prefrontal Cortex/metabolism  Interneurons/metabolism  Disease Models, Animal  Somatostatin/metabolism  Mice  Mice, Knockout  Autistic Disorder/genetics/metabolism  Social Behavior  Optogenetics  Male  Mice, Inbred C57BL  Autism Spectrum Disorder/metabolism  Magel2  Autism spectrum disorder  Medial prefrontal cortex  Social deficits  Somatostatin  procedures were performed according to the National Institutes of Health Guide  for the Care and Use of Laboratory Animals and were approved by the Animal Ethics  Committee of Zhengzhou University. Consent for publication: Not applicable.  Competing interests: The authors declare no competing interests. Index. décimale : PER Périodiques Résumé : Dysfunction in social interactions is a core symptom of autism spectrum disorder (ASD). Nevertheless, the neural mechanisms underlying social deficits in ASD are poorly understood. By integrating electrophysiological, in vivo fiber photometry, viral-mediated tracing, optogenetic and pharmacological stimulation, we show reduced intrinsic excitability and hypoactivity of SOM interneurons in medial prefrontal cortex (mPFC) in Magel2-deficient mice, an established ASD model, were required to social defects. Chemogenetic inhibition of mPFC SOM-containing interneurons resulted in reduced social interaction in wild-type Magel2 mice. These sociability deficits can be rescued by optogenetic activation by excitability of SOM in the mPFC and mPFC(SOM)-LS inhibitory pathway in Magel 2 knockout mice. These results demonstrate the hypoactivity for SOM action in the mPFC in social impairments, and suggest targeting this mechanism that may prove therapeutically beneficial for mitigating social behavioral disturbances observed in ASD. En ligne : https://dx.doi.org/10.1186/s13229-025-00653-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=555 [article] Somatostatin-expressing interneurons of prefrontal cortex modulate social deficits in the Magel2 mouse model of autism [Texte imprimé et/ou numérique] / Mengyuan CHEN, Auteur ; Daoqi MEI, Auteur ; Shengli SHI, Auteur ; Jisheng GUO, Auteur ; Chao GAO, Auteur ; Qi WANG, Auteur ; Shuai ZHAO, Auteur ; Xingxue YAN, Auteur ; Huichun ZHANG, Auteur ; Yanli WANG, Auteur ; Bin GUO, Auteur ; Yaodong ZHANG, Auteur . - 18. Langues : Anglais (eng) in Molecular Autism > 16 (2025) . - 18 Mots-clés : Animals  Prefrontal Cortex/metabolism  Interneurons/metabolism  Disease Models, Animal  Somatostatin/metabolism  Mice  Mice, Knockout  Autistic Disorder/genetics/metabolism  Social Behavior  Optogenetics  Male  Mice, Inbred C57BL  Autism Spectrum Disorder/metabolism  Magel2  Autism spectrum disorder  Medial prefrontal cortex  Social deficits  Somatostatin  procedures were performed according to the National Institutes of Health Guide  for the Care and Use of Laboratory Animals and were approved by the Animal Ethics  Committee of Zhengzhou University. Consent for publication: Not applicable.  Competing interests: The authors declare no competing interests. Index. décimale : PER Périodiques Résumé : Dysfunction in social interactions is a core symptom of autism spectrum disorder (ASD). Nevertheless, the neural mechanisms underlying social deficits in ASD are poorly understood. By integrating electrophysiological, in vivo fiber photometry, viral-mediated tracing, optogenetic and pharmacological stimulation, we show reduced intrinsic excitability and hypoactivity of SOM interneurons in medial prefrontal cortex (mPFC) in Magel2-deficient mice, an established ASD model, were required to social defects. Chemogenetic inhibition of mPFC SOM-containing interneurons resulted in reduced social interaction in wild-type Magel2 mice. These sociability deficits can be rescued by optogenetic activation by excitability of SOM in the mPFC and mPFC(SOM)-LS inhibitory pathway in Magel 2 knockout mice. These results demonstrate the hypoactivity for SOM action in the mPFC in social impairments, and suggest targeting this mechanism that may prove therapeutically beneficial for mitigating social behavioral disturbances observed in ASD. En ligne : https://dx.doi.org/10.1186/s13229-025-00653-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=555

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