کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
3042746 | 1184958 | 2016 | 12 صفحه PDF | دانلود رایگان |
• Adults with autism spectrum disorder exhibit a different pattern of neural activation (EPN) when encoding and recognizing facial expressions than neurotypical adults.
• Short serotonin transporter allele (SLC6A4) carriers have reduced neural responses (P1) during early sensory attention to facial expressions compared to long allele carriers.
• The N170, VPP and EPN, but not the P1, are influenced by emotional expressions and the EPN is the earliest component modulated by open mouths in neurotypical adults.
ObjectiveTo test differences in neural sensitivity to facial expressions, including expressions with open versus closed mouths, exhibited by (1) adults with autism spectrum disorder (ASD) compared to neurotypical adults, and by (2) short versus long serotonin transporter allele (SLC6A4) carriers.MethodsEvent related potentials (ERPs) to happy, fearful, and neutral expressions were collected from neurotypical adults (n = 25) and adults with ASD (n = 27)–of whom 32 had short and 13 had homozygous long SLC6A4 alleles.ResultsIn the neurotypical group, we confirmed that the N170, VPP and EPN, but not the P1, were influenced by emotional expressions, and determined the EPN was the earliest component modulated by open mouth. Compared to the neurotypical group, individuals with ASD exhibited differences in EPN amplitude in response to open versus closed mouths and in hemispheric distribution. Across groups, short serotonin transporter allele carriers had reduced P1 amplitude compared to long allele carriers.ConclusionsIndividuals with ASD exhibited a different pattern of neural response when encoding and recognizing facial expressions at the EPN component. Across groups, SLC6A4 allele type modulated early sensory attention at the P1.SignificanceThese results provide insight into the nature of early responses to emotional information according to genetic variation and clinical condition.
Journal: Clinical Neurophysiology - Volume 127, Issue 6, June 2016, Pages 2436–2447