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Machelska, H. et al.

Machelska, Schopohl, Mousa, Labuz, Schäfer, Stein,

Different mechanisms of intrinsic pain inhibition in early and late inflammation.

Neuroimmune interactions control pain through activation of opioid receptors on sensory nerves by immune-derived opioid peptides. Here we evaluate mechanisms of intrinsic pain inhibition at different stages of Freund's adjuvant-induced inflammation of the rat paw. We use immunohistochemistry and paw pressure testing. Our data show that in early (6 h) inflammation leukocyte-derived beta-endorphin, met-enkephalin and dynorphin A activate peripheral mu-, delta- and kappa-receptors to inhibit nociception. In addition, central opioid mechanisms seem to contribute significantly to this effect. At later stages (4 days), antinociception is exclusively produced by leukocyte-derived beta-endorphin acting at peripheral mu and delta receptors. Corticotropin-releasing hormone ( CRH) is an endogenous trigger of these effects at both stages. These findings indicate that peripheral opioid mechanisms of pain inhibition gain functional relevance with the chronicity of inflammation.[1]

References

Different mechanisms of intrinsic pain inhibition in early and late inflammation. Machelska, H., Schopohl, J.K., Mousa, S.A., Labuz, D., Schäfer, M., Stein, C. J. Neuroimmunol. (2003) [Pubmed]

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