Variation in serotonin transporter linked polymorphic region (5-HTTLPR) short/long genotype modulates resting frontal electroencephalography asymmetries in children  

Oleh:

Christou, Antonios I. ; Mccleery, Joseph P. ; Endo, Satoshi ; Wallis, Yvonne ; Bair, Hayley ; Zeegers, Maurice P.

Jenis: Article from Journal - ilmiah internasional
Dalam koleksi: Development and Psychopathology vol. 28 no. 1 (Feb. 2016), page 239-250.
Topik: 5-HTTLPR and frontal EEG asymmetries in children
Fulltext: 239-250_her.pdf (255.52KB)

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Perpustakaan Pusat (Semanggi) Nomor Panggil: DD21 Non-tandon: 1 (dapat dipinjam: 0) Tandon: tidak ada

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Previous studies have documented the serotonin transporter linked polymorphic region (5-HTTLPR) as a genetic susceptibility variant that contributes to variability in outcomes related to affective psychopathology, with the short allele associated with negative affectivity and the long allele associated with positive affectivity. In a separate but related line of research, extensive evidence suggests that frontal electroencephalography (EEG) hemispheric asymmetry in the alpha band is also associated with risk for affective psychopathologies, with leftward asymmetry associated with approach-related behavior patterns and rightward frontal EEG asymmetry associated with withdrawn behavioral tendencies. We examined frontal EEG hemispheric asymmetries in relation to 5-HTTLPR genotyping in 70 children between 4 and 6 years of age. Analyses revealed that frontal EEG lateralization interacted with genotype such that children homozygous for the short allele exhibited rightward frontal EEG asymmetries, children who were homozygous for the long allele consistently exhibited a positive pattern of leftward asymmetry, and heterozygotes exhibited equivalent left and right frontal activity. These findings suggest that the 5-HTTLPR short allele may provide a degree of susceptibility for later affective psychopathology in adolescence and adulthood, through mediation of frontal brain activity that is associated with cognitive–behavioral withdrawal tendencies and negative affectivity. There has been increasing interest in recent years in the examination of GeneEnvironment interactions in the context of developmental risk for psychiatric outcomes in humans. Based on the differential susceptibility hypothesis, individuals are differentially affected by experiences or qualities of the environment that they are exposed to over the course of development, due to preexisting heightened biological sensitivity factors (Belsky, 1997; Belsky, Bakermans-Kranenburg, & van Izendoorn, 2007). The differential susceptibility hypothesis goes beyond the description of individuals and bio- logical variables as fixed risk factors (e.g., diathesis–stress model), instead adopting the concepts of sensitivity (Boyce & Ellis, 2005) and susceptibility factors (Belsky et al., 2007) to describe complex developmental interactions among them. In addition, recent development in this model has begun to redefine “environment” as not only a range of factors originating from the external environment (Caspi et al., 2002, The first author was supported by a 3-year studentship from the Greek State Scholarships Foundation (IKY). We thank all of the families who generously participated in this study. We also thank Katherine Ellis and Rebecka Cudworth for assistance with data collection and analysis, Alena Streltsova and Lucy Wilde for assistance with data collection, and Katharine Graham for assistance in generating the social and nonsocial video stimuli. Address correspondence and reprint requests to: Joseph P. McCleery, Center for Autism Research, Children’s Hospital of Philadelphia, 3535 Market Street, #860, Philadelphia, PA 19104; E-mail: MccleeryJ@email.chop.edu. 239 2003; Fox et al., 2005

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