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Association between the oxytocin receptor (OXTR) gene and mesolimbic responses to rewards.

Publication ,  Journal Article
Damiano, CR; Aloi, J; Dunlap, K; Burrus, CJ; Mosner, MG; Kozink, RV; McLaurin, RE; Mullette-Gillman, OA; Carter, RM; Huettel, SA; McClernon, FJ ...
Published in: Mol Autism
January 31, 2014

BACKGROUND: There has been significant progress in identifying genes that confer risk for autism spectrum disorders (ASDs). However, the heterogeneity of symptom presentation in ASDs impedes the detection of ASD risk genes. One approach to understanding genetic influences on ASD symptom expression is to evaluate relations between variants of ASD candidate genes and neural endophenotypes in unaffected samples. Allelic variations in the oxytocin receptor (OXTR) gene confer small but significant risk for ASDs for which the underlying mechanisms may involve associations between variability in oxytocin signaling pathways and neural response to rewards. The purpose of this preliminary study was to investigate the influence of allelic variability in the OXTR gene on neural responses to monetary rewards in healthy adults using functional magnetic resonance imaging (fMRI). METHODS: The moderating effects of three single nucleotide polymorphisms (SNPs) (rs1042778, rs2268493 and rs237887) of the OXTR gene on mesolimbic responses to rewards were evaluated using a monetary incentive delay fMRI task. RESULTS: T homozygotes of the rs2268493 SNP demonstrated relatively decreased activation in mesolimbic reward circuitry (including the nucleus accumbens, amygdala, insula, thalamus and prefrontal cortical regions) during the anticipation of rewards but not during the outcome phase of the task. Allelic variation of the rs1042778 and rs237887 SNPs did not moderate mesolimbic activation during either reward anticipation or outcomes. CONCLUSIONS: This preliminary study suggests that the OXTR SNP rs2268493, which has been previously identified as an ASD risk gene, moderates mesolimbic responses during reward anticipation. Given previous findings of decreased mesolimbic activation during reward anticipation in ASD, the present results suggest that OXTR may confer ASD risk via influences on the neural systems that support reward anticipation.

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Published In

Mol Autism

DOI

ISSN

2040-2392

Publication Date

January 31, 2014

Volume

5

Issue

1

Start / End Page

7

Location

England

Related Subject Headings

  • 5202 Biological psychology
  • 3209 Neurosciences
  • 3202 Clinical sciences
  • 1109 Neurosciences
  • 1103 Clinical Sciences
 

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Damiano, C. R., Aloi, J., Dunlap, K., Burrus, C. J., Mosner, M. G., Kozink, R. V., … Dichter, G. S. (2014). Association between the oxytocin receptor (OXTR) gene and mesolimbic responses to rewards. Mol Autism, 5(1), 7. https://doi.org/10.1186/2040-2392-5-7
Damiano, Cara R., Joseph Aloi, Kaitlyn Dunlap, Caley J. Burrus, Maya G. Mosner, Rachel V. Kozink, Ralph Edward McLaurin, et al. “Association between the oxytocin receptor (OXTR) gene and mesolimbic responses to rewards.Mol Autism 5, no. 1 (January 31, 2014): 7. https://doi.org/10.1186/2040-2392-5-7.
Damiano CR, Aloi J, Dunlap K, Burrus CJ, Mosner MG, Kozink RV, et al. Association between the oxytocin receptor (OXTR) gene and mesolimbic responses to rewards. Mol Autism. 2014 Jan 31;5(1):7.
Damiano, Cara R., et al. “Association between the oxytocin receptor (OXTR) gene and mesolimbic responses to rewards.Mol Autism, vol. 5, no. 1, Jan. 2014, p. 7. Pubmed, doi:10.1186/2040-2392-5-7.
Damiano CR, Aloi J, Dunlap K, Burrus CJ, Mosner MG, Kozink RV, McLaurin RE, Mullette-Gillman OA, Carter RM, Huettel SA, McClernon FJ, Ashley-Koch A, Dichter GS. Association between the oxytocin receptor (OXTR) gene and mesolimbic responses to rewards. Mol Autism. 2014 Jan 31;5(1):7.
Journal cover image

Published In

Mol Autism

DOI

ISSN

2040-2392

Publication Date

January 31, 2014

Volume

5

Issue

1

Start / End Page

7

Location

England

Related Subject Headings

  • 5202 Biological psychology
  • 3209 Neurosciences
  • 3202 Clinical sciences
  • 1109 Neurosciences
  • 1103 Clinical Sciences