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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)
[article]
Titre : Annual Research Review: Development of the cerebral cortex: implications for neurodevelopmental disorders Type de document : Texte imprimé et/ou numérique 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
in Journal of Child Psychology and Psychiatry > 52-4 (April 2011) . - p.339-355[article] Annual Research Review: Development of the cerebral cortex: implications for neurodevelopmental disorders [Texte imprimé et/ou numérique] / 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 Effects of sex and DTNBP1 (dysbindin) null gene mutation on the developmental GluN2B-GluN2A switch in the mouse cortex and hippocampus / D. SINCLAIR in Journal of Neurodevelopmental Disorders, 8-1 (December 2016)
[article]
Titre : Effects of sex and DTNBP1 (dysbindin) null gene mutation on the developmental GluN2B-GluN2A switch in the mouse cortex and hippocampus Type de document : Texte imprimé et/ou numérique Auteurs : D. SINCLAIR, Auteur ; J. CESARE, Auteur ; M. MCMULLEN, Auteur ; G. C. CARLSON, Auteur ; C. G. HAHN, Auteur ; K. E. BORGMANN-WINTER, Auteur Article en page(s) : p.14 Langues : Anglais (eng) Mots-clés : Cortex Dtnbp1 Development Dysbindin GluN2B Hippocampus Nmda Phosphorylation Postsynaptic density Sex difference Index. décimale : PER Périodiques Résumé : BACKGROUND: Neurodevelopmental disorders such as autism spectrum disorders and schizophrenia differentially impact males and females and are highly heritable. The ways in which sex and genetic vulnerability influence the pathogenesis of these disorders are not clearly understood. The n-methyl-d-aspartate (NMDA) receptor pathway has been implicated in schizophrenia and autism spectrum disorders and changes dramatically across postnatal development at the level of the GluN2B-GluN2A subunit "switch" (a shift from reliance on GluN2B-containing receptors to reliance on GluN2A-containing receptors). We investigated whether sex and genetic vulnerability (specifically, null mutation of DTNBP1 [dysbindin; a possible susceptibility gene for schizophrenia]) influence the developmental GluN2B-GluN2A switch. METHODS: Subcellular fractionation to enrich for postsynaptic density (PSD), together with Western blotting and kinase assay, were used to investigate the GluN2B-GluN2A switch in the cortex and hippocampus of male and female DTNBP1 null mutant mice and their wild-type littermates. Main effects of sex and DTNBP1 genotype, and interactions with age, were assessed using factorial ANOVA. RESULTS: Sex differences in the GluN2B-GluN2A switch emerged across development at the frontal cortical synapse, in parameters related to GluN2B. Males across genotypes displayed higher GluN2B:GluN2A and GluN2B:GluN1 ratios (p < 0.05 and p < 0.01, respectively), higher GluN2B phosphorylation at Y1472 (p < 0.01), and greater abundance of PLCgamma (p < 0.01) and Fyn (p = 0.055) relative to females. In contrast, effects of DTNBP1 were evident exclusively in the hippocampus. The developmental trajectory of GluN2B was disrupted in DTNBP1 null mice (genotype x age interaction p < 0.05), which also displayed an increased synaptic GluN2A:GluN1 ratio (p < 0.05) and decreased PLCgamma (p < 0.05) and Fyn (only in females; p < 0.0005) compared to wild-types. CONCLUSIONS: Sex and DTNBP1 mutation influence the GluN2B-GluN2A switch at the synapse in a brain-region-specific fashion involving pY1472-GluN2B, Fyn, and PLCgamma. This highlights the possible mechanisms through which risk factors may mediate their effects on vulnerability to disorders of NMDA receptor dysfunction. En ligne : http://dx.doi.org/10.1186/s11689-016-9148-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.14[article] Effects of sex and DTNBP1 (dysbindin) null gene mutation on the developmental GluN2B-GluN2A switch in the mouse cortex and hippocampus [Texte imprimé et/ou numérique] / D. SINCLAIR, Auteur ; J. CESARE, Auteur ; M. MCMULLEN, Auteur ; G. C. CARLSON, Auteur ; C. G. HAHN, Auteur ; K. E. BORGMANN-WINTER, Auteur . - p.14.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 8-1 (December 2016) . - p.14
Mots-clés : Cortex Dtnbp1 Development Dysbindin GluN2B Hippocampus Nmda Phosphorylation Postsynaptic density Sex difference Index. décimale : PER Périodiques Résumé : BACKGROUND: Neurodevelopmental disorders such as autism spectrum disorders and schizophrenia differentially impact males and females and are highly heritable. The ways in which sex and genetic vulnerability influence the pathogenesis of these disorders are not clearly understood. The n-methyl-d-aspartate (NMDA) receptor pathway has been implicated in schizophrenia and autism spectrum disorders and changes dramatically across postnatal development at the level of the GluN2B-GluN2A subunit "switch" (a shift from reliance on GluN2B-containing receptors to reliance on GluN2A-containing receptors). We investigated whether sex and genetic vulnerability (specifically, null mutation of DTNBP1 [dysbindin; a possible susceptibility gene for schizophrenia]) influence the developmental GluN2B-GluN2A switch. METHODS: Subcellular fractionation to enrich for postsynaptic density (PSD), together with Western blotting and kinase assay, were used to investigate the GluN2B-GluN2A switch in the cortex and hippocampus of male and female DTNBP1 null mutant mice and their wild-type littermates. Main effects of sex and DTNBP1 genotype, and interactions with age, were assessed using factorial ANOVA. RESULTS: Sex differences in the GluN2B-GluN2A switch emerged across development at the frontal cortical synapse, in parameters related to GluN2B. Males across genotypes displayed higher GluN2B:GluN2A and GluN2B:GluN1 ratios (p < 0.05 and p < 0.01, respectively), higher GluN2B phosphorylation at Y1472 (p < 0.01), and greater abundance of PLCgamma (p < 0.01) and Fyn (p = 0.055) relative to females. In contrast, effects of DTNBP1 were evident exclusively in the hippocampus. The developmental trajectory of GluN2B was disrupted in DTNBP1 null mice (genotype x age interaction p < 0.05), which also displayed an increased synaptic GluN2A:GluN1 ratio (p < 0.05) and decreased PLCgamma (p < 0.05) and Fyn (only in females; p < 0.0005) compared to wild-types. CONCLUSIONS: Sex and DTNBP1 mutation influence the GluN2B-GluN2A switch at the synapse in a brain-region-specific fashion involving pY1472-GluN2B, Fyn, and PLCgamma. This highlights the possible mechanisms through which risk factors may mediate their effects on vulnerability to disorders of NMDA receptor dysfunction. En ligne : http://dx.doi.org/10.1186/s11689-016-9148-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=348 Strong correlation of downregulated genes related to synaptic transmission and mitochondria in post-mortem autism cerebral cortex / M. SCHWEDE in Journal of Neurodevelopmental Disorders, 10-1 (December 2018)
[article]
Titre : Strong correlation of downregulated genes related to synaptic transmission and mitochondria in post-mortem autism cerebral cortex Type de document : Texte imprimé et/ou numérique Auteurs : M. SCHWEDE, Auteur ; S. NAGPAL, Auteur ; M. J. GANDAL, Auteur ; N. N. PARIKSHAK, Auteur ; K. MIRNICS, Auteur ; D. H. GESCHWIND, Auteur ; E. M. MORROW, Auteur Année de publication : 2018 Article en page(s) : 18 p. Langues : Anglais (eng) Mots-clés : Autism Cortex Human Post-mortem Transcriptome Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic studies in autism have pinpointed a heterogeneous group of loci and genes. Further, environment may be an additional factor conferring susceptibility to autism. Transcriptome studies investigate quantitative differences in gene expression between patient-derived tissues and control. These studies may pinpoint genes relevant to pathophysiology yet circumvent the need to understand genetic architecture or gene-by-environment interactions leading to disease. METHODS: We conducted alternate gene set enrichment analyses using differentially expressed genes from a previously published RNA-seq study of post-mortem autism cerebral cortex. We used three previously published microarray datasets for validation and one of the microarray datasets for additional differential expression analysis. The RNA-seq study used 26 autism and 33 control brains in differential gene expression analysis, and the largest microarray dataset contained 15 autism and 16 control post-mortem brains. RESULTS: While performing a gene set enrichment analysis of genes differentially expressed in the RNA-seq study, we discovered that genes associated with mitochondrial function were downregulated in autism cerebral cortex, as compared to control. These genes were correlated with genes related to synaptic function. We validated these findings across the multiple microarray datasets. We also did separate differential expression and gene set enrichment analyses to confirm the importance of the mitochondrial pathway among downregulated genes in post-mortem autism cerebral cortex. CONCLUSIONS: We found that genes related to mitochondrial function were differentially expressed in autism cerebral cortex and correlated with genes related to synaptic transmission. Our principal findings replicate across all datasets investigated. Further, these findings may potentially replicate in other diseases, such as in schizophrenia. En ligne : http://dx.doi.org/10.1186/s11689-018-9237-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=386
in Journal of Neurodevelopmental Disorders > 10-1 (December 2018) . - 18 p.[article] Strong correlation of downregulated genes related to synaptic transmission and mitochondria in post-mortem autism cerebral cortex [Texte imprimé et/ou numérique] / M. SCHWEDE, Auteur ; S. NAGPAL, Auteur ; M. J. GANDAL, Auteur ; N. N. PARIKSHAK, Auteur ; K. MIRNICS, Auteur ; D. H. GESCHWIND, Auteur ; E. M. MORROW, Auteur . - 2018 . - 18 p.
Langues : Anglais (eng)
in Journal of Neurodevelopmental Disorders > 10-1 (December 2018) . - 18 p.
Mots-clés : Autism Cortex Human Post-mortem Transcriptome Index. décimale : PER Périodiques Résumé : BACKGROUND: Genetic studies in autism have pinpointed a heterogeneous group of loci and genes. Further, environment may be an additional factor conferring susceptibility to autism. Transcriptome studies investigate quantitative differences in gene expression between patient-derived tissues and control. These studies may pinpoint genes relevant to pathophysiology yet circumvent the need to understand genetic architecture or gene-by-environment interactions leading to disease. METHODS: We conducted alternate gene set enrichment analyses using differentially expressed genes from a previously published RNA-seq study of post-mortem autism cerebral cortex. We used three previously published microarray datasets for validation and one of the microarray datasets for additional differential expression analysis. The RNA-seq study used 26 autism and 33 control brains in differential gene expression analysis, and the largest microarray dataset contained 15 autism and 16 control post-mortem brains. RESULTS: While performing a gene set enrichment analysis of genes differentially expressed in the RNA-seq study, we discovered that genes associated with mitochondrial function were downregulated in autism cerebral cortex, as compared to control. These genes were correlated with genes related to synaptic function. We validated these findings across the multiple microarray datasets. We also did separate differential expression and gene set enrichment analyses to confirm the importance of the mitochondrial pathway among downregulated genes in post-mortem autism cerebral cortex. CONCLUSIONS: We found that genes related to mitochondrial function were differentially expressed in autism cerebral cortex and correlated with genes related to synaptic transmission. Our principal findings replicate across all datasets investigated. Further, these findings may potentially replicate in other diseases, such as in schizophrenia. En ligne : http://dx.doi.org/10.1186/s11689-018-9237-x Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=386 Brinp1(-/-) mice exhibit autism-like behaviour, altered memory, hyperactivity and increased parvalbumin-positive cortical interneuron density / S. R. BERKOWICZ in Molecular Autism, 7 (2016)
[article]
Titre : Brinp1(-/-) mice exhibit autism-like behaviour, altered memory, hyperactivity and increased parvalbumin-positive cortical interneuron density Type de document : Texte imprimé et/ou numérique Auteurs : S. R. BERKOWICZ, Auteur ; T. J. FEATHERBY, Auteur ; Z. QU, Auteur ; A. GIOUSOH, Auteur ; N. A. BORG, Auteur ; J. I. HENG, Auteur ; J. C. WHISSTOCK, Auteur ; P. I. BIRD, Auteur Article en page(s) : 22p. Langues : Anglais (eng) Mots-clés : Animals Attention Deficit Disorder with Hyperactivity/metabolism/pathology Autism Spectrum Disorder/metabolism/pathology Behavior, Animal Brain/metabolism/pathology Disease Models, Animal Female Genotype Glycoproteins/genetics/metabolism Interneurons/metabolism Male Memory, Short-Term Mice Mice, Inbred C57BL Mice, Knockout Motor Activity Nerve Tissue Proteins/deficiency/genetics/metabolism Parvalbumins/genetics/metabolism Phenotype Real-Time Polymerase Chain Reaction Vocalization, Animal Autism spectrum disorder Brinp1 Cortex Hyperactivity Interneuron Knock-out Neurodevelopment Parvalbumin Index. décimale : PER Périodiques Résumé : BACKGROUND: BMP/RA-inducible neural-specific protein 1 (Brinp1) is highly conserved in vertebrates, and continuously expressed in the neocortex, hippocampus, olfactory bulb and cerebellum from mid-embryonic development through to adulthood. METHODS: Brinp1 knock-out (Brinp1(-/-)) mice were generated by Cre-recombinase-mediated removal of the third exon of Brinp1. Knock-out mice were characterised by behavioural phenotyping, immunohistochemistry and expression analysis of the developing and adult brain. RESULTS: Absence of Brinp1 during development results in a behavioural phenotype resembling autism spectrum disorder (ASD), in which knock-out mice show reduced sociability and changes in vocalisation capacity. In addition, Brinp1(-/-) mice exhibit hyper-locomotor activity, have impaired short-term memory, and exhibit poor reproductive success. Brinp1(-/-) mice show increased density of parvalbumin-expressing interneurons in the adult mouse brain. Brinp1(-/-) mice do not show signs of altered neural precursor proliferation or increased apoptosis during late embryonic brain development. The expression of the related neuronal migration genes Astn1 and Astn2 is increased in the brains of Brinp1(-/-) mice, suggesting that they may ameliorate the effects of Brinp1 loss. CONCLUSIONS: Brinp1 plays an important role in normal brain development and function by influencing neuronal distribution within the cortex. The increased cortical PV-positive interneuron density and altered behaviour of Brinp1(-/-) mice resemble features of a subset of human neurological disorders; namely autism spectrum disorder (ASD) and the hyperactivity aspect of attention deficit hyperactivity disorder (ADHD). En ligne : http://dx.doi.org/10.1186/s13229-016-0079-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328
in Molecular Autism > 7 (2016) . - 22p.[article] Brinp1(-/-) mice exhibit autism-like behaviour, altered memory, hyperactivity and increased parvalbumin-positive cortical interneuron density [Texte imprimé et/ou numérique] / S. R. BERKOWICZ, Auteur ; T. J. FEATHERBY, Auteur ; Z. QU, Auteur ; A. GIOUSOH, Auteur ; N. A. BORG, Auteur ; J. I. HENG, Auteur ; J. C. WHISSTOCK, Auteur ; P. I. BIRD, Auteur . - 22p.
Langues : Anglais (eng)
in Molecular Autism > 7 (2016) . - 22p.
Mots-clés : Animals Attention Deficit Disorder with Hyperactivity/metabolism/pathology Autism Spectrum Disorder/metabolism/pathology Behavior, Animal Brain/metabolism/pathology Disease Models, Animal Female Genotype Glycoproteins/genetics/metabolism Interneurons/metabolism Male Memory, Short-Term Mice Mice, Inbred C57BL Mice, Knockout Motor Activity Nerve Tissue Proteins/deficiency/genetics/metabolism Parvalbumins/genetics/metabolism Phenotype Real-Time Polymerase Chain Reaction Vocalization, Animal Autism spectrum disorder Brinp1 Cortex Hyperactivity Interneuron Knock-out Neurodevelopment Parvalbumin Index. décimale : PER Périodiques Résumé : BACKGROUND: BMP/RA-inducible neural-specific protein 1 (Brinp1) is highly conserved in vertebrates, and continuously expressed in the neocortex, hippocampus, olfactory bulb and cerebellum from mid-embryonic development through to adulthood. METHODS: Brinp1 knock-out (Brinp1(-/-)) mice were generated by Cre-recombinase-mediated removal of the third exon of Brinp1. Knock-out mice were characterised by behavioural phenotyping, immunohistochemistry and expression analysis of the developing and adult brain. RESULTS: Absence of Brinp1 during development results in a behavioural phenotype resembling autism spectrum disorder (ASD), in which knock-out mice show reduced sociability and changes in vocalisation capacity. In addition, Brinp1(-/-) mice exhibit hyper-locomotor activity, have impaired short-term memory, and exhibit poor reproductive success. Brinp1(-/-) mice show increased density of parvalbumin-expressing interneurons in the adult mouse brain. Brinp1(-/-) mice do not show signs of altered neural precursor proliferation or increased apoptosis during late embryonic brain development. The expression of the related neuronal migration genes Astn1 and Astn2 is increased in the brains of Brinp1(-/-) mice, suggesting that they may ameliorate the effects of Brinp1 loss. CONCLUSIONS: Brinp1 plays an important role in normal brain development and function by influencing neuronal distribution within the cortex. The increased cortical PV-positive interneuron density and altered behaviour of Brinp1(-/-) mice resemble features of a subset of human neurological disorders; namely autism spectrum disorder (ASD) and the hyperactivity aspect of attention deficit hyperactivity disorder (ADHD). En ligne : http://dx.doi.org/10.1186/s13229-016-0079-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=328 Concepts neurophysiologiques du mouvement / D. DEVOS in Approche Neuropsychologique des Apprentissages chez l'Enfant - A.N.A.E., 59-60 (Novembre-Décembre 2000)
[article]
Titre : Concepts neurophysiologiques du mouvement Type de document : Texte imprimé et/ou numérique Auteurs : D. DEVOS, Auteur ; L. DEFEBVRE, Auteur Année de publication : 2000 Article en page(s) : p.138-141 Langues : Français (fre) Mots-clés : Mouvement Cortex Ganglions de la base Cervelet Organisation Index. décimale : PER Périodiques Résumé : Le mouvement nécessite une intégration complexe de nombreux systèmes moteurs, sensoriels, cérébelleux, cognitifs et émotionnels. On peut schématiquement admettre qu’au cours d’un mouvement rapide, il existe un ordre temporel d’activation de ces différentes structures nerveuses. Ainsi la première phase de planification du mouvement, où s’établit la stratégie générale de l’action, implique les aires motrices supplémentaires et les aires corticales associatives prémotrices et pariétales postérieures, puis la phase de préprogrammation des paramètres du mouvement concerne les noyaux gris centraux et le cortex cérébelleux latéral, enfin la phase d’exécution du mouvement où la volée efférente est transmise du cortex moteur vers les motoneurones via la voie corticospinale. En revanche au cours d’un tnouvement lent, il n’y aurait pas de préprogrammation et l’adaptation du mouvement serait assurée par un feed-back continu. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=198
in Approche Neuropsychologique des Apprentissages chez l'Enfant - A.N.A.E. > 59-60 (Novembre-Décembre 2000) . - p.138-141[article] Concepts neurophysiologiques du mouvement [Texte imprimé et/ou numérique] / D. DEVOS, Auteur ; L. DEFEBVRE, Auteur . - 2000 . - p.138-141.
Langues : Français (fre)
in Approche Neuropsychologique des Apprentissages chez l'Enfant - A.N.A.E. > 59-60 (Novembre-Décembre 2000) . - p.138-141
Mots-clés : Mouvement Cortex Ganglions de la base Cervelet Organisation Index. décimale : PER Périodiques Résumé : Le mouvement nécessite une intégration complexe de nombreux systèmes moteurs, sensoriels, cérébelleux, cognitifs et émotionnels. On peut schématiquement admettre qu’au cours d’un mouvement rapide, il existe un ordre temporel d’activation de ces différentes structures nerveuses. Ainsi la première phase de planification du mouvement, où s’établit la stratégie générale de l’action, implique les aires motrices supplémentaires et les aires corticales associatives prémotrices et pariétales postérieures, puis la phase de préprogrammation des paramètres du mouvement concerne les noyaux gris centraux et le cortex cérébelleux latéral, enfin la phase d’exécution du mouvement où la volée efférente est transmise du cortex moteur vers les motoneurones via la voie corticospinale. En revanche au cours d’un tnouvement lent, il n’y aurait pas de préprogrammation et l’adaptation du mouvement serait assurée par un feed-back continu. Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=198 Autism Risk Gene MET Variation and Cortical Thickness in Typically Developing Children and Adolescents / Alexis HEDRICK in Autism Research, 5-6 (December 2012)
PermalinkDistinct, dosage-sensitive requirements for the autism-associated factor CHD8 during cortical development / S. HURLEY in Molecular Autism, 12 (2021)
PermalinkThe Significance of Minicolumnar Size Variability in Autism : A Perspective from Comparative Anatomy / Manuel F. CASANOVA
PermalinkTraité de neuropsychologie clinique / Bernard LECHEVALIER
PermalinkVagus nerve stimulation as a potential adjuvant to behavioral therapy for autism and other neurodevelopmental disorders / C. T. ENGINEER in Journal of Neurodevelopmental Disorders, 9-1 (December 2017)
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