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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