Annual Research Review: Development of the cerebral cortex: implications for neurodevelopmental disorders / John L.R. RUBENSTEIN in Journal of Child Psychology and Psychiatry, 52-4 (April 2011)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 52-4 (April 2011) . - p.339-355 Titre : Annual Research Review: Development of the cerebral cortex: implications for neurodevelopmental disorders Type de document : texte imprimé Auteurs : John L.R. RUBENSTEIN, Auteur Année de publication : 2011 Article en page(s) : p.339-355 Langues : Anglais (eng) Mots-clés : Cortex  development  autism  brain development  fibroblast growth factor  GABA Index. décimale : PER Périodiques Résumé : The cerebral cortex has a central role in cognitive and emotional processing. As such, understanding the mechanisms that govern its development and function will be central to understanding the bases of severe neuropsychiatric disorders, particularly those that first appear in childhood. In this review, I highlight recent progress in elucidating genetic, molecular and cellular mechanisms that control cortical development. I discuss basic aspects of cortical developmental anatomy, and mechanisms that regulate cortical size and area formation, with an emphasis on the roles of fibroblast growth factor (Fgf) signaling and specific transcription factors. I then examine how specific types of cortical excitatory projection neurons are generated, and how their axons grow along stereotyped pathways to their targets. Next, I address how cortical inhibitory (GABAergic) neurons are generated, and point out the role of these cells in controlling cortical plasticity and critical periods. The paper concludes with an examination of four possible developmental mechanisms that could contribute to some forms of neurodevelopmental disorders, such as autism. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2010.02307.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=119 [article] Annual Research Review: Development of the cerebral cortex: implications for neurodevelopmental disorders [texte imprimé] / John L.R. RUBENSTEIN, Auteur . - 2011 . - p.339-355. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 52-4 (April 2011) . - p.339-355 Mots-clés : Cortex  development  autism  brain development  fibroblast growth factor  GABA Index. décimale : PER Périodiques Résumé : The cerebral cortex has a central role in cognitive and emotional processing. As such, understanding the mechanisms that govern its development and function will be central to understanding the bases of severe neuropsychiatric disorders, particularly those that first appear in childhood. In this review, I highlight recent progress in elucidating genetic, molecular and cellular mechanisms that control cortical development. I discuss basic aspects of cortical developmental anatomy, and mechanisms that regulate cortical size and area formation, with an emphasis on the roles of fibroblast growth factor (Fgf) signaling and specific transcription factors. I then examine how specific types of cortical excitatory projection neurons are generated, and how their axons grow along stereotyped pathways to their targets. Next, I address how cortical inhibitory (GABAergic) neurons are generated, and point out the role of these cells in controlling cortical plasticity and critical periods. The paper concludes with an examination of four possible developmental mechanisms that could contribute to some forms of neurodevelopmental disorders, such as autism. En ligne : http://dx.doi.org/10.1111/j.1469-7610.2010.02307.x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=119

Developmental Neurobiology of Autism Spectrum Disorders / John L.R. RUBENSTEIN

Public ISBD in Autism Spectrum Disorders / David G. AMARAL Titre : Developmental Neurobiology of Autism Spectrum Disorders Type de document : texte imprimé Auteurs : John L.R. RUBENSTEIN, Auteur Année de publication : 2011 Importance : p.527-538 Langues : Anglais (eng) 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=139 in Autism Spectrum Disorders / David G. AMARAL Developmental Neurobiology of Autism Spectrum Disorders [texte imprimé] / John L.R. RUBENSTEIN, Auteur . - 2011 . - p.527-538. Langues : Anglais (eng) 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=139

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Erratum to: Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development / Mario MAIRA in Journal of Neurodevelopmental Disorders, 2-1 (March 2010)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 2-1 (March 2010) . - p.47 Titre : Erratum to: Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development Type de document : texte imprimé Auteurs : Mario MAIRA, Auteur ; Jason E. LONG, Auteur ; Amie Y. LEE, Auteur ; John L.R. RUBENSTEIN, Auteur ; Stefano STIFANI, Auteur Article en page(s) : p.47 Langues : Anglais (eng) Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-009-9040-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342 [article] Erratum to: Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development [texte imprimé] / Mario MAIRA, Auteur ; Jason E. LONG, Auteur ; Amie Y. LEE, Auteur ; John L.R. RUBENSTEIN, Auteur ; Stefano STIFANI, Auteur . - p.47. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 2-1 (March 2010) . - p.47 Index. décimale : PER Périodiques En ligne : http://dx.doi.org/10.1007/s11689-009-9040-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=342

LiCl treatment leads to long-term restoration of spine maturation and synaptogenesis in adult Tbr1 mutants / Siavash FAZEL DARBANDI in Journal of Neurodevelopmental Disorders, 14 (2022)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 14 (2022) Titre : LiCl treatment leads to long-term restoration of spine maturation and synaptogenesis in adult Tbr1 mutants Type de document : texte imprimé Auteurs : Siavash FAZEL DARBANDI, Auteur ; Andrew D. NELSON, Auteur ; Emily Ling-Lin PAI, Auteur ; Kevin J. BENDER, Auteur ; John L.R. RUBENSTEIN, Auteur Langues : Anglais (eng) Mots-clés : Animals  Autism Spectrum Disorder/genetics  Humans  Mice  Neurogenesis/physiology  Neurons  Synaptic Transmission  T-Box Domain Proteins/genetics  Transcription Factors  Autism spectrum disorder  Cortex  Dendritic spine  Excitatory neuron  Synaptic rescue  Synaptogenesis  Tbr1  mPFCx  Neurona, a company studying the potential therapeutic use of interneuron  transplantation. The other authors declare that they have no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Tbr1 encodes a T-box transcription factor and is considered a high confidence autism spectrum disorder (ASD) gene. Tbr1 is expressed in the postmitotic excitatory neurons of the deep neocortical layers 5 and 6. Postnatally and neonatally, Tbr1 conditional mutants (CKOs) have immature dendritic spines and reduced synaptic density. However, an understanding of Tbr1's function in the adult mouse brain remains elusive. METHODS: We used conditional mutagenesis to interrogate Tbr1's function in cortical layers 5 and 6 of the adult mouse cortex. RESULTS: Adult Tbr1 CKO mutants have dendritic spine and synaptic deficits as well as reduced frequency of mEPSCs and mIPSCs. LiCl, a WNT signaling agonist, robustly rescues the dendritic spine maturation, synaptic defects, and excitatory and inhibitory synaptic transmission deficits. CONCLUSIONS: LiCl treatment could be used as a therapeutic approach for some cases of ASD with deficits in synaptic transmission. En ligne : https://dx.doi.org/10.1186/s11689-022-09421-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=574 [article] LiCl treatment leads to long-term restoration of spine maturation and synaptogenesis in adult Tbr1 mutants [texte imprimé] / Siavash FAZEL DARBANDI, Auteur ; Andrew D. NELSON, Auteur ; Emily Ling-Lin PAI, Auteur ; Kevin J. BENDER, Auteur ; John L.R. RUBENSTEIN, Auteur. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 14 (2022) Mots-clés : Animals  Autism Spectrum Disorder/genetics  Humans  Mice  Neurogenesis/physiology  Neurons  Synaptic Transmission  T-Box Domain Proteins/genetics  Transcription Factors  Autism spectrum disorder  Cortex  Dendritic spine  Excitatory neuron  Synaptic rescue  Synaptogenesis  Tbr1  mPFCx  Neurona, a company studying the potential therapeutic use of interneuron  transplantation. The other authors declare that they have no competing interests. Index. décimale : PER Périodiques Résumé : BACKGROUND: Tbr1 encodes a T-box transcription factor and is considered a high confidence autism spectrum disorder (ASD) gene. Tbr1 is expressed in the postmitotic excitatory neurons of the deep neocortical layers 5 and 6. Postnatally and neonatally, Tbr1 conditional mutants (CKOs) have immature dendritic spines and reduced synaptic density. However, an understanding of Tbr1's function in the adult mouse brain remains elusive. METHODS: We used conditional mutagenesis to interrogate Tbr1's function in cortical layers 5 and 6 of the adult mouse cortex. RESULTS: Adult Tbr1 CKO mutants have dendritic spine and synaptic deficits as well as reduced frequency of mEPSCs and mIPSCs. LiCl, a WNT signaling agonist, robustly rescues the dendritic spine maturation, synaptic defects, and excitatory and inhibitory synaptic transmission deficits. CONCLUSIONS: LiCl treatment could be used as a therapeutic approach for some cases of ASD with deficits in synaptic transmission. En ligne : https://dx.doi.org/10.1186/s11689-022-09421-5 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=574

Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons / Rong MAO in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.224-36 Titre : Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons Type de document : texte imprimé Auteurs : Rong MAO, Auteur ; Damon T. PAGE, Auteur ; Irina MERZLYAK, Auteur ; Carol KIM, Auteur ; Laurence H. TECOTT, Auteur ; Patricia H. JANAK, Auteur ; John L.R. RUBENSTEIN, Auteur ; Mriganka SUR, Auteur Article en page(s) : p.224-36 Langues : Anglais (eng) Mots-clés : Associative learning  Behavior  Calretinin  Fear conditioning  GABAergic  Hyperactivity  Inhibitory  Interneuron  Neuropsychiatric disease  Prepulse inhibition Index. décimale : PER Périodiques Résumé : UNLABELLED: The inhibitory GABAergic system has been implicated in multiple neuropsychiatric diseases such as schizophrenia and autism. The Dlx homeobox transcription factor family is essential for development and function of GABAergic interneurons. Mice lacking the Dlx1 gene have postnatal subtype-specific loss of interneurons and reduced IPSCs in their cortex and hippocampus. To ascertain consequences of these changes in the GABAergic system, we performed a battery of behavioral assays on the Dlx1 mutant mice, including zero maze, open field, locomotor activity, food intake, rotarod, tail suspension, fear conditioning assays (context and trace), prepulse inhibition, and working memory related tasks (spontaneous alteration task and spatial working memory task). Dlx1 mutant mice displayed elevated activity levels in open field, locomotor activity, and tail suspension tests. These mice also showed deficits in contextual and trace fear conditioning, and possibly in prepulse inhibition. Their learning deficits were not global, as the mutant mice did not differ from the wild-type controls in tests of working memory. Our findings demonstrate a critical role for the Dlx1 gene, and likely the subclasses of interneurons that are affected by the lack of this gene, in behavioral inhibition and associative fear learning. These observations support the involvement of particular components of the GABAergic system in specific behavioral phenotypes related to complex neuropsychiatric diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9025-8) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9025-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] Reduced conditioned fear response in mice that lack Dlx1 and show subtype-specific loss of interneurons [texte imprimé] / Rong MAO, Auteur ; Damon T. PAGE, Auteur ; Irina MERZLYAK, Auteur ; Carol KIM, Auteur ; Laurence H. TECOTT, Auteur ; Patricia H. JANAK, Auteur ; John L.R. RUBENSTEIN, Auteur ; Mriganka SUR, Auteur . - p.224-36. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.224-36 Mots-clés : Associative learning  Behavior  Calretinin  Fear conditioning  GABAergic  Hyperactivity  Inhibitory  Interneuron  Neuropsychiatric disease  Prepulse inhibition Index. décimale : PER Périodiques Résumé : UNLABELLED: The inhibitory GABAergic system has been implicated in multiple neuropsychiatric diseases such as schizophrenia and autism. The Dlx homeobox transcription factor family is essential for development and function of GABAergic interneurons. Mice lacking the Dlx1 gene have postnatal subtype-specific loss of interneurons and reduced IPSCs in their cortex and hippocampus. To ascertain consequences of these changes in the GABAergic system, we performed a battery of behavioral assays on the Dlx1 mutant mice, including zero maze, open field, locomotor activity, food intake, rotarod, tail suspension, fear conditioning assays (context and trace), prepulse inhibition, and working memory related tasks (spontaneous alteration task and spatial working memory task). Dlx1 mutant mice displayed elevated activity levels in open field, locomotor activity, and tail suspension tests. These mice also showed deficits in contextual and trace fear conditioning, and possibly in prepulse inhibition. Their learning deficits were not global, as the mutant mice did not differ from the wild-type controls in tests of working memory. Our findings demonstrate a critical role for the Dlx1 gene, and likely the subclasses of interneurons that are affected by the lack of this gene, in behavioral inhibition and associative fear learning. These observations support the involvement of particular components of the GABAergic system in specific behavioral phenotypes related to complex neuropsychiatric diseases. ELECTRONIC SUPPLEMENTARY MATERIAL: The online version of this article (doi:10.1007/s11689-009-9025-8) contains supplementary material, which is available to authorized users. En ligne : http://dx.doi.org/10.1007/s11689-009-9025-8 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Role for TGF-beta superfamily signaling in telencephalic GABAergic neuron development / Mario MAIRA in Journal of Neurodevelopmental Disorders, 2-1 (March 2010)  

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Transcriptomic metaanalyses of autistic brains reveals shared gene expression and biological pathway abnormalities with cancer / J. FORES-MARTOS in Molecular Autism, 10 (2019)  

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