A functional polymorphism of the brain derived neurotrophic factor gene and cortical anatomy in autism spectrum disorder / A. RAZNAHAN in Journal of Neurodevelopmental Disorders, 1-3 (September 2009)  

Public ISBD [article]  inJournal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.215-23 Titre : A functional polymorphism of the brain derived neurotrophic factor gene and cortical anatomy in autism spectrum disorder Type de document : Texte imprimé et/ou numérique Auteurs : A. RAZNAHAN, Auteur ; R. TORO, Auteur ; P. PROITSI, Auteur ; J. POWELL, Auteur ; T. PAUS, Auteur ; Patrick BOLTON, Auteur ; D. G. MURPHY, Auteur Article en page(s) : p.215-23 Langues : Anglais (eng) Index. décimale : PER Périodiques Résumé : Autism Spectrum Disorder (ASD) is associated with both (i) post-mortem and neuroimaging evidence of abnormal cortical development, and (ii) altered signalling in Brain Derived Neurotrophic Factor (BDNF) pathways - which regulate neuroproliferative and neuroplastic processes. In healthy controls genotype at a single nucleotide polymorphism that alters BDNF signalling (Val66met) has been related to regional cortical volume. It is not known however if this influence on brain development is intact in ASD. Therefore we compared the relationship between genotype and cortical anatomy (as measured using in vivo Magnetic Resonance Imaging) in 41 people with ASD and 30 healthy controls. We measured cortical volume, and its two sole determinants - cortical thickness and surface area - which reflect differing neurodevelopmental processes. We found "Group-by-Genotype" interactions for cortical volume in medial (caudal anterior cingulate, posterior cingulate) and lateral (rostral middle, lateral orbitofrontal, pars orbitalis and pars triangularis) frontal cortices. Furthermore, within (only) these regions "Group-by-Genotype" interactions were also found for surface area. No effects were found for cortical thickness in any region. Our preliminary findings suggest that people with ASD have differences from controls in the relationship between BDNF val66met genotype and regional (especially frontal) cortical volume and surface area, but not cortical thickness. Therefore alterations in the relationship between BDNF val66met genotype and surface area in ASD may drive the findings for volume. If correct, this suggests ASD is associated with a distorted relationship between BDNF val66met genotype and the determinants of regional cortical surface area - gyrification and/or sulcal positioning. En ligne : http://dx.doi.org/10.1007/s11689-009-9012-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341 [article] A functional polymorphism of the brain derived neurotrophic factor gene and cortical anatomy in autism spectrum disorder [Texte imprimé et/ou numérique] / A. RAZNAHAN, Auteur ; R. TORO, Auteur ; P. PROITSI, Auteur ; J. POWELL, Auteur ; T. PAUS, Auteur ; Patrick BOLTON, Auteur ; D. G. MURPHY, Auteur . - p.215-23. Langues : Anglais (eng) in Journal of Neurodevelopmental Disorders > 1-3 (September 2009) . - p.215-23 Index. décimale : PER Périodiques Résumé : Autism Spectrum Disorder (ASD) is associated with both (i) post-mortem and neuroimaging evidence of abnormal cortical development, and (ii) altered signalling in Brain Derived Neurotrophic Factor (BDNF) pathways - which regulate neuroproliferative and neuroplastic processes. In healthy controls genotype at a single nucleotide polymorphism that alters BDNF signalling (Val66met) has been related to regional cortical volume. It is not known however if this influence on brain development is intact in ASD. Therefore we compared the relationship between genotype and cortical anatomy (as measured using in vivo Magnetic Resonance Imaging) in 41 people with ASD and 30 healthy controls. We measured cortical volume, and its two sole determinants - cortical thickness and surface area - which reflect differing neurodevelopmental processes. We found "Group-by-Genotype" interactions for cortical volume in medial (caudal anterior cingulate, posterior cingulate) and lateral (rostral middle, lateral orbitofrontal, pars orbitalis and pars triangularis) frontal cortices. Furthermore, within (only) these regions "Group-by-Genotype" interactions were also found for surface area. No effects were found for cortical thickness in any region. Our preliminary findings suggest that people with ASD have differences from controls in the relationship between BDNF val66met genotype and regional (especially frontal) cortical volume and surface area, but not cortical thickness. Therefore alterations in the relationship between BDNF val66met genotype and surface area in ASD may drive the findings for volume. If correct, this suggests ASD is associated with a distorted relationship between BDNF val66met genotype and the determinants of regional cortical surface area - gyrification and/or sulcal positioning. En ligne : http://dx.doi.org/10.1007/s11689-009-9012-0 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=341

Methylation of OPRL1 mediates the effect of psychosocial stress on binge drinking in adolescents / B. RUGGERI in Journal of Child Psychology and Psychiatry, 59-6 (June 2018)  

Public ISBD [article]  inJournal of Child Psychology and Psychiatry > 59-6 (June 2018) . - p.650-658 Titre : Methylation of OPRL1 mediates the effect of psychosocial stress on binge drinking in adolescents Type de document : Texte imprimé et/ou numérique Auteurs : B. RUGGERI, Auteur ; C. MACARE, Auteur ; S. STOPPONI, Auteur ; T. JIA, Auteur ; F. M. CARVALHO, Auteur ; G. ROBERT, Auteur ; Tobias BANASCHEWSKI, Auteur ; Arun L. W. BOKDE, Auteur ; Uli BROMBERG, Auteur ; C. BUCHEL, Auteur ; A. CATTRELL, Auteur ; P. J. CONROD, Auteur ; S. DESRIVIERES, Auteur ; H. FLOR, Auteur ; V. FROUIN, Auteur ; J. GALLINAT, Auteur ; H. GARAVAN, Auteur ; P. GOWLAND, Auteur ; A. HEINZ, Auteur ; B. ITTERMANN, Auteur ; J. L. MARTINOT, Auteur ; M. P. MARTINOT, Auteur ; F. NEES, Auteur ; D. PAPADOPOULOS-ORFANOS, Auteur ; T. PAUS, Auteur ; L. POUSTKA, Auteur ; M. N. SMOLKA, Auteur ; N. C. VETTER, Auteur ; H. WALTER, Auteur ; R. WHELAN, Auteur ; W. H. SOMMER, Auteur ; G. BAKALKIN, Auteur ; R. CICCOCIOPPO, Auteur ; G. SCHUMANN, Auteur Article en page(s) : p.650-658 Langues : Anglais (eng) Mots-clés : OPRL1 methylation  adolescence  binge drinking  nucleus accumbens  stressful life events Index. décimale : PER Périodiques Résumé : BACKGROUND: Nociceptin is a key regulator linking environmental stress and alcohol drinking. In a genome-wide methylation analysis, we recently identified an association of a methylated region in the OPRL1 gene with alcohol-use disorders. METHODS: Here, we investigate the biological basis of this observation by analysing psychosocial stressors, methylation of the OPRL1 gene, brain response during reward anticipation and alcohol drinking in 660 fourteen-year-old adolescents of the IMAGEN study. We validate our findings in marchigian sardinian (msP) alcohol-preferring rats that are genetically selected for increased alcohol drinking and stress sensitivity. RESULTS: We found that low methylation levels in intron 1 of OPRL1 are associated with higher psychosocial stress and higher frequency of binge drinking, an effect mediated by OPRL1 methylation. In individuals with low methylation of OPRL1, frequency of binge drinking is associated with stronger BOLD response in the ventral striatum during reward anticipation. In msP rats, we found that stress results in increased alcohol intake and decreased methylation of OPRL1 in the nucleus accumbens. CONCLUSIONS: Our findings describe an epigenetic mechanism that helps to explain how psychosocial stress influences risky alcohol consumption and reward processing, thus contributing to the elucidation of biological mechanisms underlying risk for substance abuse. En ligne : http://dx.doi.org/10.1111/jcpp.12843 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=363 [article] Methylation of OPRL1 mediates the effect of psychosocial stress on binge drinking in adolescents [Texte imprimé et/ou numérique] / B. RUGGERI, Auteur ; C. MACARE, Auteur ; S. STOPPONI, Auteur ; T. JIA, Auteur ; F. M. CARVALHO, Auteur ; G. ROBERT, Auteur ; Tobias BANASCHEWSKI, Auteur ; Arun L. W. BOKDE, Auteur ; Uli BROMBERG, Auteur ; C. BUCHEL, Auteur ; A. CATTRELL, Auteur ; P. J. CONROD, Auteur ; S. DESRIVIERES, Auteur ; H. FLOR, Auteur ; V. FROUIN, Auteur ; J. GALLINAT, Auteur ; H. GARAVAN, Auteur ; P. GOWLAND, Auteur ; A. HEINZ, Auteur ; B. ITTERMANN, Auteur ; J. L. MARTINOT, Auteur ; M. P. MARTINOT, Auteur ; F. NEES, Auteur ; D. PAPADOPOULOS-ORFANOS, Auteur ; T. PAUS, Auteur ; L. POUSTKA, Auteur ; M. N. SMOLKA, Auteur ; N. C. VETTER, Auteur ; H. WALTER, Auteur ; R. WHELAN, Auteur ; W. H. SOMMER, Auteur ; G. BAKALKIN, Auteur ; R. CICCOCIOPPO, Auteur ; G. SCHUMANN, Auteur . - p.650-658. Langues : Anglais (eng) in Journal of Child Psychology and Psychiatry > 59-6 (June 2018) . - p.650-658 Mots-clés : OPRL1 methylation  adolescence  binge drinking  nucleus accumbens  stressful life events Index. décimale : PER Périodiques Résumé : BACKGROUND: Nociceptin is a key regulator linking environmental stress and alcohol drinking. In a genome-wide methylation analysis, we recently identified an association of a methylated region in the OPRL1 gene with alcohol-use disorders. METHODS: Here, we investigate the biological basis of this observation by analysing psychosocial stressors, methylation of the OPRL1 gene, brain response during reward anticipation and alcohol drinking in 660 fourteen-year-old adolescents of the IMAGEN study. We validate our findings in marchigian sardinian (msP) alcohol-preferring rats that are genetically selected for increased alcohol drinking and stress sensitivity. RESULTS: We found that low methylation levels in intron 1 of OPRL1 are associated with higher psychosocial stress and higher frequency of binge drinking, an effect mediated by OPRL1 methylation. In individuals with low methylation of OPRL1, frequency of binge drinking is associated with stronger BOLD response in the ventral striatum during reward anticipation. In msP rats, we found that stress results in increased alcohol intake and decreased methylation of OPRL1 in the nucleus accumbens. CONCLUSIONS: Our findings describe an epigenetic mechanism that helps to explain how psychosocial stress influences risky alcohol consumption and reward processing, thus contributing to the elucidation of biological mechanisms underlying risk for substance abuse. En ligne : http://dx.doi.org/10.1111/jcpp.12843 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=363

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