3 recherche sur le mot-clé 'Optogenetics'

Epilogue: Perspectives and Caveats / Pierre L. ROUBERTOUX

Public ISBD in Organism models of autism spectrum disorders / Pierre L. ROUBERTOUX Titre : Epilogue: Perspectives and Caveats Type de document : texte imprimé Auteurs : Pierre L. ROUBERTOUX, Auteur Année de publication : 2015 Importance : p.471-477 Langues : Anglais (eng) Mots-clés : Induced pluripotent stem cells (iPSC)  Bacteria  Optogenetics  Susceptibility genes  Treatments Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=265 in Organism models of autism spectrum disorders / Pierre L. ROUBERTOUX Epilogue: Perspectives and Caveats [texte imprimé] / Pierre L. ROUBERTOUX, Auteur . - 2015 . - p.471-477. Langues : Anglais (eng) Mots-clés : Induced pluripotent stem cells (iPSC)  Bacteria  Optogenetics  Susceptibility genes  Treatments Index. décimale : AUT-B AUT-B - L'Autisme - Ouvrages généraux et scientifiques Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=265

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Human Inducible Pluripotent Stem Cells and Autism Spectrum Disorder: Emerging Technologies / Andre W. PHILLIPS ; Elena ARTIMOVICH ; Jonathan E. NESTOR ; John P. HUSSMAN ; Gene J. BLATT in Autism Research, 9-5 (May 2016)  

Public ISBD [article]  inAutism Research > 9-5 (May 2016) . - p.513-535 Titre : Human Inducible Pluripotent Stem Cells and Autism Spectrum Disorder: Emerging Technologies Type de document : texte imprimé Auteurs : Andre W. PHILLIPS, Auteur ; Elena ARTIMOVICH, Auteur ; Jonathan E. NESTOR, Auteur ; John P. HUSSMAN, Auteur ; Gene J. BLATT, Auteur Article en page(s) : p.513-535 Langues : Anglais (eng) Mots-clés : human stem cells  autism  drug-screening  high-throughput  inducible pluripotent stem cells  CRISPR  optogenetics  organoids Index. décimale : PER Périodiques Résumé : Autism Spectrum Disorder (ASD) is a behaviorally defined neurodevelopmental condition. Symptoms of ASD cover the spectrum from mild qualitative differences in social interaction to severe communication and social and behavioral challenges that require lifelong support. Attempts at understanding the pathophysiology of ASD have been hampered by a multifactorial etiology that stretches the limits of current behavioral and cell based models. Recent progress has implicated numerous autism-risk genes but efforts to gain a better understanding of the underlying biological mechanisms have seen slow progress. This is in part due to lack of appropriate models for complete molecular and pharmacological studies. The advent of induced pluripotent stem cells (iPSC) has reinvigorated efforts to establish more complete model systems that more reliably identify molecular pathways and predict effective drug targets and candidates in ASD. iPSCs are particularly appealing because they can be derived from human patients and controls for research purposes and provide a technology for the development of a personalized treatment regimen for ASD patients. The pluripotency of iPSCs allow them to be reprogrammed into a number of CNS cell types and phenotypically screened across many patients. This quality is already being exploited in protocols to generate 2-dimensional (2-D) and three-dimensional (3-D) models of neurons and developing brain structures. iPSC models make powerful platforms that can be interrogated using electrophysiology, gene expression studies, and other cell-based quantitative assays. iPSC technology has limitations but when combined with other model systems has great potential for helping define the underlying pathophysiology of ASD. En ligne : http://dx.doi.org/10.1002/aur.1570 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=289 [article] Human Inducible Pluripotent Stem Cells and Autism Spectrum Disorder: Emerging Technologies [texte imprimé] / Andre W. PHILLIPS, Auteur ; Elena ARTIMOVICH, Auteur ; Jonathan E. NESTOR, Auteur ; John P. HUSSMAN, Auteur ; Gene J. BLATT, Auteur . - p.513-535. Langues : Anglais (eng) in Autism Research > 9-5 (May 2016) . - p.513-535 Mots-clés : human stem cells  autism  drug-screening  high-throughput  inducible pluripotent stem cells  CRISPR  optogenetics  organoids Index. décimale : PER Périodiques Résumé : Autism Spectrum Disorder (ASD) is a behaviorally defined neurodevelopmental condition. Symptoms of ASD cover the spectrum from mild qualitative differences in social interaction to severe communication and social and behavioral challenges that require lifelong support. Attempts at understanding the pathophysiology of ASD have been hampered by a multifactorial etiology that stretches the limits of current behavioral and cell based models. Recent progress has implicated numerous autism-risk genes but efforts to gain a better understanding of the underlying biological mechanisms have seen slow progress. This is in part due to lack of appropriate models for complete molecular and pharmacological studies. The advent of induced pluripotent stem cells (iPSC) has reinvigorated efforts to establish more complete model systems that more reliably identify molecular pathways and predict effective drug targets and candidates in ASD. iPSCs are particularly appealing because they can be derived from human patients and controls for research purposes and provide a technology for the development of a personalized treatment regimen for ASD patients. The pluripotency of iPSCs allow them to be reprogrammed into a number of CNS cell types and phenotypically screened across many patients. This quality is already being exploited in protocols to generate 2-dimensional (2-D) and three-dimensional (3-D) models of neurons and developing brain structures. iPSC models make powerful platforms that can be interrogated using electrophysiology, gene expression studies, and other cell-based quantitative assays. iPSC technology has limitations but when combined with other model systems has great potential for helping define the underlying pathophysiology of ASD. En ligne : http://dx.doi.org/10.1002/aur.1570 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=289

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 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] / 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