Modulation of Peripheral Endogenous Opioid Analgesia by Central Afferent Blockade

Schmitt, Thomas K.; Mousa, Shaaban A.; Brack, Alexander; Schmidt, D; Rittner, Heike L.; Welte, M.; Schäfer, Michael; Stein, Christoph

doi:10.1097/00000542-200301000-00030

Cited by 45 publications

(29 citation statements)

References 24 publications

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“…In addition, the recruitment of opioid-containing cells is dependent on neurokinin-1 receptors (which bind substance P) (Rittner et al, 2007b), on sensory and sympathetic neurons (Kager et al, 2010), and may be regulated by adhesion to neurons (Hua et al, 2006). Central mechanisms also play a role because intrathecally administered analgesic doses of morphine led to a decreased number of END-positive leukocytes in inflamed rat paws (Schmitt et al, 2003). This was confirmed in a clinical study using epidural analgesia in patients undergoing surgery (Heurich et al, 2007).…”

Section: Migration Of Opioid Peptide-producing Cells Tomentioning

confidence: 87%

“…Thus, adhesion molecules have an impact on pain by modulating the extravasation of opioid producing immune cells and/or their adhesion to sensory neurons. In addition, central mechanisms apparently influence the migration of opioid-containing cells and endogenous analgesia in peripheral injured tissue (Schmitt et al, 2003;Heurich et al, 2007).…”

Section: Intrinsic Induction Of Opioid Peptide Release From Inflammatmentioning

confidence: 99%

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Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

2011

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Section: Migration Of Opioid Peptide-producing Cells Tomentioning

confidence: 87%

Section: Intrinsic Induction Of Opioid Peptide Release From Inflammatmentioning

confidence: 99%

Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

2011

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“…Endogenous opioids may act by modulating pain at peripheral and central levels (13). Many studies have demonstrated an increase in the plasma levels of endogenous opioids, mostly β-endorphin, during and after aerobic exercise (5); however, only a few studies have investigated alterations in this parameter when resistance exercise was involved, with equivocal results.…”

Section: Discussionmentioning

confidence: 99%

Participation of endogenous opioids in the antinociception induced by resistance exercise in rats

Galdino

Duarte

Perez

2010

Braz J Med Biol Res

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“…catheterization was performed as described elsewhere with slight modifications (Schmitt et al, 2003;Strkson et al, 1996). Briefly, an incision was made at the L3-L4 level.…”

Section: Surgery To Implant Icv or It Guide Cannulamentioning

confidence: 99%

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

Mousa

Bopaiah

Richter

et al. 2007

Neuropsychopharmacol

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There is conflicting evidence on the antinociceptive effects of corticotropin-releasing factor (CRF) along the neuraxis of pain transmission and the responsible anatomical sites of CRF's action at the level of the brain, spinal cord and periphery. In an animal model of tonic pain, that is, Freunds complete adjuvant (FCA) hindpaw inflammation, we systematically investigated CRF's ability to modulate inflammatory pain at those three levels of pain transmission by algesiometry following the intracerebroventricular, intrathecal, and intraplantar application of low, systemically inactive doses of CRF. At each level, CRF elicits potent antinociceptive effects, which are dose dependent and antagonized by local, but not systemic CRF receptor antagonist a-helical CRF indicating CRF receptor specificity. Consistently, we have identified by immunohistochemistry multiple brain areas, inhibitory interneurons within the dorsal horn of the spinal cord as well as immune cells within subcutaneous tissueFbut not peripheral sensory neuronsFthat coexpress both CRF receptors and opioid peptides. In line with these anatomical findings, local administration of CRF together with the opioid receptor antagonist naloxone dosedependently reversed CRF's antinociceptive effects at each of these three levels of pain transmission. Therefore, local application of low, systemically inactive doses of CRF at the level of the brain, spinal cord and periphery inhibits tonic inflammatory pain most likely through an activation of CRF receptors on cells that coexpress opioid peptides which results in opioid-mediated pain inhibition. Future studies have to delineate whether endogenous CRF at these three levels contributes to the body's response to cope with the stressful stimulus pain in an opioid-mediated manner.

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Modulation of Peripheral Endogenous Opioid Analgesia by Central Afferent Blockade

Abstract: These findings suggest an interplay of central and peripheral mechanisms of pain control. An effective central inhibition of pain apparently signals a reduced need for recruitment of opioid-containing immune cells to injured sites.

Cited by 45 publications

References 24 publications

Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

Modulation of Peripheral Sensory Neurons by the Immune System: Implications for Pain Therapy

Participation of endogenous opioids in the antinociception induced by resistance exercise in rats

Inhibition of Inflammatory Pain by CRF at Peripheral, Spinal and Supraspinal Sites: Involvement of Areas Coexpressing CRF Receptors and Opioid Peptides

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