The genetic influence on the cortical processing of experimental pain and the moderating effect of pain status.
<h4>Background</h4>Research suggests that the COMT Val(158)Met, BDNF Val(66)Met and OPRM1 A(118)G polymorphisms moderate the experience of pain. In order to obtain experimental confirmation and extension of findings, cortical processing of experimentally-induced pain was used.<h4>M...
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| Autores principales: | , , , , , |
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| Formato: | article |
| Lenguaje: | EN |
| Publicado: |
Public Library of Science (PLoS)
2010
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| Materias: | |
| Acceso en línea: | https://doaj.org/article/513e2eb67fbb44588dbedf2b6192ea11 |
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| Sumario: | <h4>Background</h4>Research suggests that the COMT Val(158)Met, BDNF Val(66)Met and OPRM1 A(118)G polymorphisms moderate the experience of pain. In order to obtain experimental confirmation and extension of findings, cortical processing of experimentally-induced pain was used.<h4>Method</h4>A sample of 78 individuals with chronic low back pain complaints and 37 healthy controls underwent EEG registration. Event-Related Potentials were measured in response to electrical nociceptive stimuli and moderation by COMT Val(158)Met, BDNF Val(66)Met and OPRM1 A(118)G polymorphisms was assessed.<h4>Results</h4>Genetic variation did not have a direct effect on cortical processing of experimental pain. However, genetic effects (COMT Val(158)Met and BDNF Val(66)Met) on experimental pain were moderated by the presence of chronic pain. In the presence of chronic pain, the COMT Met allele and the BDNF Met allele augmented cortical pain processing, whilst reducing pain processing in pain-free controls. No significant effects were found concerning the OPRM1 A(118)G polymorphism.<h4>Conclusions</h4>The current study suggests that chronic experience of pain enhances genetic sensitivity to experimentally induced mildly painful stimuli, possibly through a process of epigenetic modification. |
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