Pain activation of human supraspinal opioid pathways as demonstrated by [11C]-carfentanil and positron emission tomography (PET)

Bencherif, Badreddine; Fuchs, Perry N.; Sheth, Rishi N.; Dannals, Robert F.; Campbell, James N.; Frost, J. James

doi:10.1016/s0304-3959(02)00266-x

Cited by 124 publications

(78 citation statements)

References 59 publications

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“…Conversely, [11C]diprenorphine BP in components of the affective pain network was significantly increased in a cohort of patients after surgical relief of trigeminal neuralgia pain [14], consistent with the hypothesis that relief of pain is associated with decreased endogenous opioid release. Recent studies using a high affinity muselective opiate agonist, [11C]carfentanil, and PET have demonstrated decreased mu opioid receptor BP in the thalamus and amygdala following administration of acute experimental noxious stimuli consistent with the hypothesis of pain-induced release of endogenous opioid peptides [2,48].…”

Section: Discussionmentioning

confidence: 66%

A combined [11C]diprenorphine PET study and fMRI study of acupuncture analgesia

Dougherty

Kong

Webb

et al. 2008

Behavioural Brain Research

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Functional neuroimaging studies suggest that a lateral network in the brain is associated with the sensory aspects of pain perception while a medial network is associated with affective aspects. The highest concentration of opioid receptors is in the medial network. There is significant evidence that endogenous opioids are central to the experience of pain and analgesia. We applied an integrative multimodal imaging approach during acupuncture. We found functional magnetic resonance imaging signal changes in the orbitofrontal cortex, insula, and pons and [11C]diprenorphine positron emission tomography signal changes in the orbitofrontal cortex, medial prefrontal cortex, insula, thalamus, and anterior cingulate cortex. These findings include brain regions within both the lateral and medial pain networks.

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Section: Discussionmentioning

confidence: 66%

A combined [11C]diprenorphine PET study and fMRI study of acupuncture analgesia

Dougherty

Kong

Webb

et al. 2008

Behavioural Brain Research

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“…In emotionally-neutral states, the bioavailability of µ-opioid receptors in the posterior thalamus is lower in women with MDD than in nondepressed controls, consistent with chronic over-activity of the opioid system in MDD [30]. Bioavailability of µ-opioid receptors decreases in this part of the brain during painful stimulation [7,50], presumably due to pain-induced release of endogenous opioids.…”

Section: Stress-induced Analgesiamentioning

confidence: 81%

Stress-evoked opioid release inhibits pain in major depressive disorder

Frew

Drummond

2008

Pain

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To determine whether stress-evoked release of endogenous opioids might account for hypoalgesia in major depressive disorder (MDD), the µ-opioid antagonist naltrexone (50 mg) or placebo was administered double-blind to 24 participants with MDD and to 31 non-depressed controls. Eighty minutes later participants completed a painful foot cold pressor test and, after a 5-minute interval, began a 25-minute arithmetic task interspersed with painful electric shocks. Ten minutes later participants completed a second cold pressor test. Negative affect was greater in participants with MDD than in non-depressed controls throughout the experiment, and increased significantly in both groups during mental arithmetic. Before the math task, naltrexone unmasked direct linear relationships between severity of depression, negative affect while resting quietly, and cold-induced pain in participants with MDD. In contrast, facilitatory effects of naltrexone on cold-and shock-induced pain were greatest in controls with the lowest depression scores. Naltrexone strengthened the relationship between negative affect and shock-induced pain during the math task, particularly in the depressed group, and heightened anxiety in both groups toward the end of the task. Thus, µ-opioid activity apparently masked a positive association between negative affect and pain in the most distressed participants. These findings suggest that psychological distress inhibits pain via stress-evoked release of opioid peptides in severe cases of MDD. In addition, tonic endogenous opioid neurotransmission could inhibit depressive symptoms and pain in people with low depression scores.

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“…Under these conditions, activation of this neurotransmitter system is evidenced by reductions in the in vivo availability of synaptic -opioid receptors to bind the radiolabeled tracer (Zubieta et al, 2001(Zubieta et al, , 2002(Zubieta et al, , 2003bBencherif et al, 2002).…”

Section: The Pharmacological Approachmentioning

confidence: 99%