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Genetic variation in serotonin transporter modulates tactile hyperresponsiveness in ASD / Kimberly B. SCHAUDER in Research in Autism Spectrum Disorders, 10 (February 2015)
[article]
Titre : Genetic variation in serotonin transporter modulates tactile hyperresponsiveness in ASD Type de document : Texte imprimé et/ou numérique Auteurs : Kimberly B. SCHAUDER, Auteur ; Christopher L. MULLER, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur ; Carissa J. CASCIO, Auteur Article en page(s) : p.93-100 Langues : Anglais (eng) Mots-clés : SERT Tactile hyperresponsiveness Sensory processing Autism spectrum disorder Index. décimale : PER Périodiques Résumé : Several lines of evidence implicate dysfunction of the serotonin (5-HT) system in autism spectrum disorder (ASD). Specifically, the serotonin transporter (5-HTT, SERT) has been scrutinized as an ASD candidate risk gene. SERT plays key roles in the development of circuits that underlie sensory function, particularly in the somatosensory system. One previous study in ASD found association of a rare, hyperfunctional SERT variant with sensory aversion, but studies of common SERT variants have never examined sensory symptoms in ASD. Using standardized caregiver assessments of sensory function in children, we evaluated patterns of sensory responsiveness in 47 children with ASD and 38 typically developing (TD) children. Study participants were genotyped for the functional SERT promoter polymorphisms, 5-HTTLPR and rs25531, to test the hypothesis that the higher expressing genotypes would be associated with hyperresponsiveness to touch, a common sensory aversion in ASD. All measures of sensory hypo- and hyperresponsiveness were increased in children with ASD, with hyporesponsive sensory patterns negatively correlated to age and hyperresponsive sensory patterns positively correlated to repetitive behavior. Strikingly, high-expressing SERT genotypes were associated with increased tactile hyperresponsiveness in the ASD group. Our findings indicate genetic variation that increases SERT function may specifically impact somatosensory processing in ASD. En ligne : http://dx.doi.org/10.1016/j.rasd.2014.11.008 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=260
in Research in Autism Spectrum Disorders > 10 (February 2015) . - p.93-100[article] Genetic variation in serotonin transporter modulates tactile hyperresponsiveness in ASD [Texte imprimé et/ou numérique] / Kimberly B. SCHAUDER, Auteur ; Christopher L. MULLER, Auteur ; Jeremy VEENSTRA-VANDERWEELE, Auteur ; Carissa J. CASCIO, Auteur . - p.93-100.
Langues : Anglais (eng)
in Research in Autism Spectrum Disorders > 10 (February 2015) . - p.93-100
Mots-clés : SERT Tactile hyperresponsiveness Sensory processing Autism spectrum disorder Index. décimale : PER Périodiques Résumé : Several lines of evidence implicate dysfunction of the serotonin (5-HT) system in autism spectrum disorder (ASD). Specifically, the serotonin transporter (5-HTT, SERT) has been scrutinized as an ASD candidate risk gene. SERT plays key roles in the development of circuits that underlie sensory function, particularly in the somatosensory system. One previous study in ASD found association of a rare, hyperfunctional SERT variant with sensory aversion, but studies of common SERT variants have never examined sensory symptoms in ASD. Using standardized caregiver assessments of sensory function in children, we evaluated patterns of sensory responsiveness in 47 children with ASD and 38 typically developing (TD) children. Study participants were genotyped for the functional SERT promoter polymorphisms, 5-HTTLPR and rs25531, to test the hypothesis that the higher expressing genotypes would be associated with hyperresponsiveness to touch, a common sensory aversion in ASD. All measures of sensory hypo- and hyperresponsiveness were increased in children with ASD, with hyporesponsive sensory patterns negatively correlated to age and hyperresponsive sensory patterns positively correlated to repetitive behavior. Strikingly, high-expressing SERT genotypes were associated with increased tactile hyperresponsiveness in the ASD group. Our findings indicate genetic variation that increases SERT function may specifically impact somatosensory processing in ASD. En ligne : http://dx.doi.org/10.1016/j.rasd.2014.11.008 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=260 Serotonin neuron abnormalities in the BTBR mouse model of autism / Yue-Ping GUO in Autism Research, 10-1 (January 2017)
[article]
Titre : Serotonin neuron abnormalities in the BTBR mouse model of autism Type de document : Texte imprimé et/ou numérique Auteurs : Yue-Ping GUO, Auteur ; Kathryn G. COMMONS, Auteur Article en page(s) : p.66-77 Langues : Anglais (eng) Mots-clés : dorsal raphel median raphe hippocampus monoamine norepinephrine SERT swim Index. décimale : PER Périodiques Résumé : The inbred mouse strain BTBR T+ Itpr3tf/J (BTBR) is studied as a model of idiopathic autism because they are less social and more resistant to change than other strains. Forebrain serotonin receptors and the response to serotonin drugs are altered in BTBR mice, yet it remains unknown if serotonin neurons themselves are abnormal. In this study, we found that serotonin tissue content and the density of serotonin axons is reduced in the hippocampus of BTBR mice in comparison to C57BL/6J (C57) mice. This was accompanied by possible compensatory changes in serotonin neurons that were most pronounced in regions known to provide innervation to the hippocampus: the caudal dorsal raphe (B6) and the median raphe. These changes included increased numbers of serotonin neurons and hyperactivation of Fos expression. Metrics of serotonin neurons in the rostral 2/3 of the dorsal raphe and serotonin content of the prefrontal cortex were less impacted. Thus, serotonin neurons exhibit region-dependent abnormalities in the BTBR mouse that may contribute to their altered behavioral profile. En ligne : http://dx.doi.org/10.1002/aur.1665 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=302
in Autism Research > 10-1 (January 2017) . - p.66-77[article] Serotonin neuron abnormalities in the BTBR mouse model of autism [Texte imprimé et/ou numérique] / Yue-Ping GUO, Auteur ; Kathryn G. COMMONS, Auteur . - p.66-77.
Langues : Anglais (eng)
in Autism Research > 10-1 (January 2017) . - p.66-77
Mots-clés : dorsal raphel median raphe hippocampus monoamine norepinephrine SERT swim Index. décimale : PER Périodiques Résumé : The inbred mouse strain BTBR T+ Itpr3tf/J (BTBR) is studied as a model of idiopathic autism because they are less social and more resistant to change than other strains. Forebrain serotonin receptors and the response to serotonin drugs are altered in BTBR mice, yet it remains unknown if serotonin neurons themselves are abnormal. In this study, we found that serotonin tissue content and the density of serotonin axons is reduced in the hippocampus of BTBR mice in comparison to C57BL/6J (C57) mice. This was accompanied by possible compensatory changes in serotonin neurons that were most pronounced in regions known to provide innervation to the hippocampus: the caudal dorsal raphe (B6) and the median raphe. These changes included increased numbers of serotonin neurons and hyperactivation of Fos expression. Metrics of serotonin neurons in the rostral 2/3 of the dorsal raphe and serotonin content of the prefrontal cortex were less impacted. Thus, serotonin neurons exhibit region-dependent abnormalities in the BTBR mouse that may contribute to their altered behavioral profile. En ligne : http://dx.doi.org/10.1002/aur.1665 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=302