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The serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces
Previous research has found that a common polymorphism in the serotonin transporter gene (5-HTTLPR) is an important mediator of individual differences in brain responses associated with emotional behaviour. In particular, relative to individuals homozygous for the l-allele, carriers of the s-allele...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Pergamon Press
2011
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209561/ https://www.ncbi.nlm.nih.gov/pubmed/21167188 http://dx.doi.org/10.1016/j.neuropsychologia.2010.12.013 |
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author | von dem Hagen, Elisabeth A.H. Passamonti, Luca Nutland, Sarah Sambrook, Jennifer Calder, Andrew J. |
author_facet | von dem Hagen, Elisabeth A.H. Passamonti, Luca Nutland, Sarah Sambrook, Jennifer Calder, Andrew J. |
author_sort | von dem Hagen, Elisabeth A.H. |
collection | PubMed |
description | Previous research has found that a common polymorphism in the serotonin transporter gene (5-HTTLPR) is an important mediator of individual differences in brain responses associated with emotional behaviour. In particular, relative to individuals homozygous for the l-allele, carriers of the s-allele display heightened amygdala activation to emotional compared to non-emotional stimuli. However, there is some debate as to whether this difference is driven by increased activation to emotional stimuli, resting baseline differences between the groups, or decreased activation to neutral stimuli. We performed functional imaging during an implicit facial expression processing task in which participants viewed angry, sad and neutral faces. In addition to neutral faces, we included two further baseline conditions, houses and fixation. We found increased amygdala activation in s-allele carriers relative to l-homozygotes in response to angry faces compared to neutral faces, houses and fixation. When comparing neutral faces to houses or fixation, we found no significant difference in amygdala response between the two groups. In addition, there was no significant difference between the groups in response to fixation when compared with a houses baseline. Overall, these results suggest that the increased amygdala response observed in s-allele carriers to emotional faces is primarily driven by an increased response to emotional faces rather than a decreased response to neutral faces or an increased resting baseline. The results are discussed in relation to the tonic and phasic hypotheses of 5-HTTLPR-mediated modulation of amygdala activity. |
format | Online Article Text |
id | pubmed-3209561 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2011 |
publisher | Pergamon Press |
record_format | MEDLINE/PubMed |
spelling | pubmed-32095612011-12-28 The serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces von dem Hagen, Elisabeth A.H. Passamonti, Luca Nutland, Sarah Sambrook, Jennifer Calder, Andrew J. Neuropsychologia Article Previous research has found that a common polymorphism in the serotonin transporter gene (5-HTTLPR) is an important mediator of individual differences in brain responses associated with emotional behaviour. In particular, relative to individuals homozygous for the l-allele, carriers of the s-allele display heightened amygdala activation to emotional compared to non-emotional stimuli. However, there is some debate as to whether this difference is driven by increased activation to emotional stimuli, resting baseline differences between the groups, or decreased activation to neutral stimuli. We performed functional imaging during an implicit facial expression processing task in which participants viewed angry, sad and neutral faces. In addition to neutral faces, we included two further baseline conditions, houses and fixation. We found increased amygdala activation in s-allele carriers relative to l-homozygotes in response to angry faces compared to neutral faces, houses and fixation. When comparing neutral faces to houses or fixation, we found no significant difference in amygdala response between the two groups. In addition, there was no significant difference between the groups in response to fixation when compared with a houses baseline. Overall, these results suggest that the increased amygdala response observed in s-allele carriers to emotional faces is primarily driven by an increased response to emotional faces rather than a decreased response to neutral faces or an increased resting baseline. The results are discussed in relation to the tonic and phasic hypotheses of 5-HTTLPR-mediated modulation of amygdala activity. Pergamon Press 2011-03 /pmc/articles/PMC3209561/ /pubmed/21167188 http://dx.doi.org/10.1016/j.neuropsychologia.2010.12.013 Text en © 2011 Elsevier Ltd. https://creativecommons.org/licenses/by/3.0/ Open Access under CC BY 3.0 (https://creativecommons.org/licenses/by/3.0/) license |
spellingShingle | Article von dem Hagen, Elisabeth A.H. Passamonti, Luca Nutland, Sarah Sambrook, Jennifer Calder, Andrew J. The serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces |
title | The serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces |
title_full | The serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces |
title_fullStr | The serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces |
title_full_unstemmed | The serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces |
title_short | The serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces |
title_sort | serotonin transporter gene polymorphism and the effect of baseline on amygdala response to emotional faces |
topic | Article |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3209561/ https://www.ncbi.nlm.nih.gov/pubmed/21167188 http://dx.doi.org/10.1016/j.neuropsychologia.2010.12.013 |
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