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Emotion Potentiated Startle in Fragile X Syndrome / Elizabeth C. BALLINGER in Journal of Autism and Developmental Disorders, 44-10 (October 2014)
[article]
Titre : Emotion Potentiated Startle in Fragile X Syndrome Type de document : Texte imprimé et/ou numérique Auteurs : Elizabeth C. BALLINGER, Auteur ; Lisa CORDEIRO, Auteur ; Alyssa D. CHAVEZ, Auteur ; Randi J. HAGERMAN, Auteur ; David HESSL, Auteur Article en page(s) : p.2536-2546 Langues : Anglais (eng) Mots-clés : Fragile X syndrome Social anxiety Amygdala Startle Autism Index. décimale : PER Périodiques Résumé : Social avoidance and anxiety are prevalent in fragile X syndrome (FXS) and are potentially mediated by the amygdala, a brain region critical for social behavior. Unfortunately, functional brain resonance imaging investigation of the amygdala in FXS is limited by the difficulties experienced by intellectually impaired and anxious participants. We investigated the relationship between social avoidance and emotion-potentiated startle, a probe of amygdala activation, in children and adolescents with FXS, developmental disability without FXS (DD), and typical development. Individuals with FXS or DD demonstrated significantly reduced potentiation to fearful faces than a typically developing control group (p .05). However, among individuals with FXS, social avoidance correlated positively with fearful-face potentiation (p .05). This suggests that general intellectual disability blunts amygdalar response, but differential amygdala responsiveness to social stimuli contributes to phenotypic variability among individuals with FXS. En ligne : http://dx.doi.org/10.1007/s10803-014-2125-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=240
in Journal of Autism and Developmental Disorders > 44-10 (October 2014) . - p.2536-2546[article] Emotion Potentiated Startle in Fragile X Syndrome [Texte imprimé et/ou numérique] / Elizabeth C. BALLINGER, Auteur ; Lisa CORDEIRO, Auteur ; Alyssa D. CHAVEZ, Auteur ; Randi J. HAGERMAN, Auteur ; David HESSL, Auteur . - p.2536-2546.
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 44-10 (October 2014) . - p.2536-2546
Mots-clés : Fragile X syndrome Social anxiety Amygdala Startle Autism Index. décimale : PER Périodiques Résumé : Social avoidance and anxiety are prevalent in fragile X syndrome (FXS) and are potentially mediated by the amygdala, a brain region critical for social behavior. Unfortunately, functional brain resonance imaging investigation of the amygdala in FXS is limited by the difficulties experienced by intellectually impaired and anxious participants. We investigated the relationship between social avoidance and emotion-potentiated startle, a probe of amygdala activation, in children and adolescents with FXS, developmental disability without FXS (DD), and typical development. Individuals with FXS or DD demonstrated significantly reduced potentiation to fearful faces than a typically developing control group (p .05). However, among individuals with FXS, social avoidance correlated positively with fearful-face potentiation (p .05). This suggests that general intellectual disability blunts amygdalar response, but differential amygdala responsiveness to social stimuli contributes to phenotypic variability among individuals with FXS. En ligne : http://dx.doi.org/10.1007/s10803-014-2125-7 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=240 Brief Report: Sensorimotor Gating in Idiopathic Autism and Autism Associated with Fragile X Syndrome / Jennifer YUHAS in Journal of Autism and Developmental Disorders, 41-2 (February 2011)
[article]
Titre : Brief Report: Sensorimotor Gating in Idiopathic Autism and Autism Associated with Fragile X Syndrome Type de document : Texte imprimé et/ou numérique Auteurs : Jennifer YUHAS, Auteur ; Lisa CORDEIRO, Auteur ; Flora TASSONE, Auteur ; Elizabeth C. BALLINGER, Auteur ; Andrea SCHNEIDER, Auteur ; James M. LONG, Auteur ; Edward M. ORNITZ, Auteur ; David HESSL, Auteur Année de publication : 2011 Article en page(s) : p.248-253 Note générale : Article Open Access Langues : Anglais (eng) Mots-clés : PPI FMR1 gene Sensorimotor gating mGluR5 Prepulse inhibition Startle Index. décimale : PER Périodiques Résumé : Prepulse inhibition (PPI) may useful for exploring the proposed shared neurobiology between idiopathic autism and autism caused by FXS. We compared PPI in four groups: typically developing controls (n = 18), FXS and autism (FXS+A; n = 15), FXS without autism spectrum disorder (FXS−A; n = 17), and idiopathic autism (IA; n = 15). Relative to controls, the FXS+A (p < 0.002) and FXS−A (p < 0.003) groups had impaired PPI. The FXS+A (p < 0.01) and FXS−A (p < 0.03) groups had lower PPI than the IA group. Prolonged startle latency was seen in the IA group. The differing PPI profiles seen in the FXS+A and IA indicates these groups may not share a common neurobiological abnormality of sensorimotor gating. En ligne : http://dx.doi.org/10.1007/s10803-010-1040-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=117
in Journal of Autism and Developmental Disorders > 41-2 (February 2011) . - p.248-253[article] Brief Report: Sensorimotor Gating in Idiopathic Autism and Autism Associated with Fragile X Syndrome [Texte imprimé et/ou numérique] / Jennifer YUHAS, Auteur ; Lisa CORDEIRO, Auteur ; Flora TASSONE, Auteur ; Elizabeth C. BALLINGER, Auteur ; Andrea SCHNEIDER, Auteur ; James M. LONG, Auteur ; Edward M. ORNITZ, Auteur ; David HESSL, Auteur . - 2011 . - p.248-253.
Article Open Access
Langues : Anglais (eng)
in Journal of Autism and Developmental Disorders > 41-2 (February 2011) . - p.248-253
Mots-clés : PPI FMR1 gene Sensorimotor gating mGluR5 Prepulse inhibition Startle Index. décimale : PER Périodiques Résumé : Prepulse inhibition (PPI) may useful for exploring the proposed shared neurobiology between idiopathic autism and autism caused by FXS. We compared PPI in four groups: typically developing controls (n = 18), FXS and autism (FXS+A; n = 15), FXS without autism spectrum disorder (FXS−A; n = 17), and idiopathic autism (IA; n = 15). Relative to controls, the FXS+A (p < 0.002) and FXS−A (p < 0.003) groups had impaired PPI. The FXS+A (p < 0.01) and FXS−A (p < 0.03) groups had lower PPI than the IA group. Prolonged startle latency was seen in the IA group. The differing PPI profiles seen in the FXS+A and IA indicates these groups may not share a common neurobiological abnormality of sensorimotor gating. En ligne : http://dx.doi.org/10.1007/s10803-010-1040-9 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=117 Loss of Cntnap2 in the Rat Causes Autism-Related Alterations in Social Interactions, Stereotypic Behavior, and Sensory Processing / Kaela E. SCOTT in Autism Research, 13-10 (October 2020)
[article]
Titre : Loss of Cntnap2 in the Rat Causes Autism-Related Alterations in Social Interactions, Stereotypic Behavior, and Sensory Processing Type de document : Texte imprimé et/ou numérique Auteurs : Kaela E. SCOTT, Auteur ; Karnig KAZAZIAN, Auteur ; Rajkamalpreet S. MANN, Auteur ; Dorit MÖHRLE, Auteur ; Ashley L. SCHORMANS, Auteur ; Susanne SCHMID, Auteur ; Brian L. ALLMAN, Auteur Article en page(s) : p.1698-1717 Langues : Anglais (eng) Mots-clés : Cntnap2 animal model autism spectrum disorder behavior sensory social startle Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is characterized by social interaction and communication impairments, as well as restrictive/repetitive patterns of behavior, interests or activities, which can coexist with intellectual disability and altered sensory processing. To study the mechanisms underlying these core features of ASD, preclinical research has developed animal models with manipulations in ASD-linked genes, such as CNTNAP2. In order to fully interpret the findings from mechanistic studies, the extent to which these models display behaviors consistent with ASD must be determined. Toward that goal, we conducted an investigation of the consequences of a functional loss of Cntnap2 on ASD-related behaviors by comparing the performance of rats with a homozygous or heterozygous knockout of Cntnap2 to their wildtype littermates across a comprehensive test battery. Cntnap2(-/-) rats showed deficits in sociability and social novelty, and they displayed repetitive circling and hyperlocomotion. Moreover, Cntnap2(-/-) rats demonstrated exaggerated acoustic startle responses, increased avoidance to sounds of moderate intensity, and a lack of rapid audiovisual temporal recalibration; indicating changes in sensory processing at both the pre-attentive and perceptual levels. Notably, sensory behaviors requiring learned associations did not reveal genotypic differences, whereas tasks relying on automatic/implicit behaviors did. Ultimately, because these collective alterations in social, stereotypic, and sensory behaviors are phenotypically similar to those reported in individuals with ASD, our results establish the Cntnap2 knockout rat model as an effective platform to study not only the molecular and cellular mechanisms associated with ASD, but also the complex relationship between altered sensory processing and other core ASD-related behaviors. LAY SUMMARY: Autism spectrum disorder (ASD) is characterized by social interaction differences, and restrictive/repetitive patterns of behavior. We studied the behavioral alterations caused by the loss of an autism-linked gene, Cntnap2, in the rat to determine how mutations in this gene contribute to autism-related behaviors. We show the loss of Cntnap2 leads to changes in social, stereotypic, and sensory behaviors, indicating this rat model can be used to better understand the brain changes underlying ASD. Autism Res 2020, 13: 1698-1717. © 2020 International Society for Autism Research and Wiley Periodicals LLC. En ligne : http://dx.doi.org/10.1002/aur.2364 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=431
in Autism Research > 13-10 (October 2020) . - p.1698-1717[article] Loss of Cntnap2 in the Rat Causes Autism-Related Alterations in Social Interactions, Stereotypic Behavior, and Sensory Processing [Texte imprimé et/ou numérique] / Kaela E. SCOTT, Auteur ; Karnig KAZAZIAN, Auteur ; Rajkamalpreet S. MANN, Auteur ; Dorit MÖHRLE, Auteur ; Ashley L. SCHORMANS, Auteur ; Susanne SCHMID, Auteur ; Brian L. ALLMAN, Auteur . - p.1698-1717.
Langues : Anglais (eng)
in Autism Research > 13-10 (October 2020) . - p.1698-1717
Mots-clés : Cntnap2 animal model autism spectrum disorder behavior sensory social startle Index. décimale : PER Périodiques Résumé : Autism spectrum disorder (ASD) is characterized by social interaction and communication impairments, as well as restrictive/repetitive patterns of behavior, interests or activities, which can coexist with intellectual disability and altered sensory processing. To study the mechanisms underlying these core features of ASD, preclinical research has developed animal models with manipulations in ASD-linked genes, such as CNTNAP2. In order to fully interpret the findings from mechanistic studies, the extent to which these models display behaviors consistent with ASD must be determined. Toward that goal, we conducted an investigation of the consequences of a functional loss of Cntnap2 on ASD-related behaviors by comparing the performance of rats with a homozygous or heterozygous knockout of Cntnap2 to their wildtype littermates across a comprehensive test battery. Cntnap2(-/-) rats showed deficits in sociability and social novelty, and they displayed repetitive circling and hyperlocomotion. Moreover, Cntnap2(-/-) rats demonstrated exaggerated acoustic startle responses, increased avoidance to sounds of moderate intensity, and a lack of rapid audiovisual temporal recalibration; indicating changes in sensory processing at both the pre-attentive and perceptual levels. Notably, sensory behaviors requiring learned associations did not reveal genotypic differences, whereas tasks relying on automatic/implicit behaviors did. Ultimately, because these collective alterations in social, stereotypic, and sensory behaviors are phenotypically similar to those reported in individuals with ASD, our results establish the Cntnap2 knockout rat model as an effective platform to study not only the molecular and cellular mechanisms associated with ASD, but also the complex relationship between altered sensory processing and other core ASD-related behaviors. LAY SUMMARY: Autism spectrum disorder (ASD) is characterized by social interaction differences, and restrictive/repetitive patterns of behavior. We studied the behavioral alterations caused by the loss of an autism-linked gene, Cntnap2, in the rat to determine how mutations in this gene contribute to autism-related behaviors. We show the loss of Cntnap2 leads to changes in social, stereotypic, and sensory behaviors, indicating this rat model can be used to better understand the brain changes underlying ASD. Autism Res 2020, 13: 1698-1717. © 2020 International Society for Autism Research and Wiley Periodicals LLC. En ligne : http://dx.doi.org/10.1002/aur.2364 Permalink : https://www.cra-rhone-alpes.org/cid/opac_css/index.php?lvl=notice_display&id=431