Journal article
The effect of opioid receptor blockade on the neural processing of thermal stimuli.
- Abstract:
- The endogenous opioid system represents one of the principal systems in the modulation of pain. This has been demonstrated in studies of placebo analgesia and stress-induced analgesia, where anti-nociceptive activity triggered by pain itself or by cognitive states is blocked by opioid antagonists. The aim of this study was to characterize the effect of opioid receptor blockade on the physiological processing of painful thermal stimulation in the absence of cognitive manipulation. We therefore measured BOLD (blood oxygen level dependent) signal responses and intensity ratings to non-painful and painful thermal stimuli in a double-blind, cross-over design using the opioid receptor antagonist naloxone. On the behavioral level, we observed an increase in intensity ratings under naloxone due mainly to a difference in the non-painful stimuli. On the neural level, painful thermal stimulation was associated with a negative BOLD signal within the pregenual anterior cingulate cortex, and this deactivation was abolished by naloxone.
- Publication status:
- Published
- Peer review status:
- Peer reviewed
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(Preview, Version of record, pdf, 1.2MB, Terms of use)
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- Publisher copy:
- 10.1371/journal.pone.0012344
Authors
- Publisher:
- Public Library of Science
- Journal:
- PloS one More from this journal
- Volume:
- 5
- Issue:
- 8
- Article number:
- e12344
- Publication date:
- 2010-01-01
- DOI:
- EISSN:
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1932-6203
- Language:
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English
- Keywords:
- Pubs id:
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241730
- UUID:
-
uuid:034c6368-cbe7-48ac-918f-ed78d40c3ac6
- Local pid:
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pubs:241730
- Source identifiers:
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241730
- Deposit date:
-
2012-12-19
- ARK identifier:
Terms of use
- Copyright holder:
- Schoell et al
- Copyright date:
- 2010
- Notes:
- Copyright 2010 Schoell et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
- Licence:
- CC Attribution (CC BY)
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