<HashMap><database>biostudies-literature</database><scores><citationCount>0</citationCount><reanalysisCount>0</reanalysisCount><viewCount>63</viewCount><searchCount>0</searchCount></scores><additional><submitter>Wiggins JL</submitter><funding>NICHD NIH HHS</funding><funding>NCRR NIH HHS</funding><funding>NIMH NIH HHS</funding><funding>NIDCD NIH HHS</funding><funding>NINDS NIH HHS</funding><pagination>832-8</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC4040086</full_dataset_link><repository>biostudies-literature</repository><omics_type>Unknown</omics_type><volume>9(6)</volume><pubmed_abstract>Failure of the amygdala to habituate, or decrease response intensity, to repeatedly presented faces may be one mechanism by which individuals with autism spectrum disorders (ASD) develop and maintain social symptoms. However, genetic influences on habituation in ASD have not been examined. We hypothesized that serotonin transporter-linked promoter region (5-HTTLPR) genotype affects change in amygdala response to repeated sad faces differently in individuals with ASD vs healthy controls. Forty-four youth with ASD and 65 controls aged 8-19 years were genotyped and underwent an event-related functional magnetic resonance imaging scan where they identified the gender of emotional faces presented for 250 ms. The first half of the run was compared with the second half to assess habituation. 5-HTTLPR genotype influences amygdala habituation to sad faces differently for individuals with ASD vs controls. The genotype-by-diagnosis-by-run half interaction was driven by individuals with ASD and low expressing genotypes (S/S, S/L(G) and L(G)/L(G)), who trended toward sensitization (increase in amygdala activation) and whose habituation scores significantly differed from individuals with ASD and higher expressing genotypes (L(A)/L(A), S/L(A) and L(A)/L(G)) as well as controls with low expressing genotypes. Our results show that amygdala response to social stimuli in ASD, which may contribute to social symptoms, is genetically influenced.</pubmed_abstract><journal>Social cognitive and affective neuroscience</journal><pubmed_title>Serotonin transporter genotype impacts amygdala habituation in youth with autism spectrum disorders.</pubmed_title><pmcid>PMC4040086</pmcid><funding_grant_id>R01 MH066496</funding_grant_id><funding_grant_id>U19HD35482</funding_grant_id><funding_grant_id>R01DC009410</funding_grant_id><funding_grant_id>UL1 RR024986</funding_grant_id><funding_grant_id>R01 NS054784</funding_grant_id><funding_grant_id>R01 DC009410</funding_grant_id><funding_grant_id>UL1RR024986</funding_grant_id><funding_grant_id>MH066496</funding_grant_id><funding_grant_id>R01NS54784</funding_grant_id><funding_grant_id>U19 HD035482</funding_grant_id><pubmed_authors>Martin DM</pubmed_authors><pubmed_authors>Swartz JR</pubmed_authors><pubmed_authors>Wiggins JL</pubmed_authors><pubmed_authors>Lord C</pubmed_authors><pubmed_authors>Monk CS</pubmed_authors><view_count>63</view_count></additional><is_claimable>false</is_claimable><name>Serotonin transporter genotype impacts amygdala habituation in youth with autism spectrum disorders.</name><description>Failure of the amygdala to habituate, or decrease response intensity, to repeatedly presented faces may be one mechanism by which individuals with autism spectrum disorders (ASD) develop and maintain social symptoms. However, genetic influences on habituation in ASD have not been examined. We hypothesized that serotonin transporter-linked promoter region (5-HTTLPR) genotype affects change in amygdala response to repeated sad faces differently in individuals with ASD vs healthy controls. Forty-four youth with ASD and 65 controls aged 8-19 years were genotyped and underwent an event-related functional magnetic resonance imaging scan where they identified the gender of emotional faces presented for 250 ms. The first half of the run was compared with the second half to assess habituation. 5-HTTLPR genotype influences amygdala habituation to sad faces differently for individuals with ASD vs controls. The genotype-by-diagnosis-by-run half interaction was driven by individuals with ASD and low expressing genotypes (S/S, S/L(G) and L(G)/L(G)), who trended toward sensitization (increase in amygdala activation) and whose habituation scores significantly differed from individuals with ASD and higher expressing genotypes (L(A)/L(A), S/L(A) and L(A)/L(G)) as well as controls with low expressing genotypes. Our results show that amygdala response to social stimuli in ASD, which may contribute to social symptoms, is genetically influenced.</description><dates><release>2014-01-01T00:00:00Z</release><publication>2014 Jun</publication><modification>2024-11-13T09:44:06.698Z</modification><creation>2019-03-27T01:29:11Z</creation></dates><accession>S-EPMC4040086</accession><cross_references><pubmed>23526151</pubmed><doi>10.1093/scan/nst039</doi></cross_references></HashMap>