Different mechanisms of intrinsic pain inhibition in early and late inflammation

Different mechanisms of intrinsic pain inhibition in early and late inflammation

Machelska H; Schopohl JK; Mousa SA; Labuz D; Schafer M; Stein C

Journal Of Neuroimmunology

2003

Male; Time Factors; Pain Threshold; Animals; Rats; Biomarkers of Pain; Injections; Subcutaneous; Enkephalin; Hindlimb; Wistar; Corticotropin-Releasing Hormone/administration & dosage; Dynorphins/antagonists & inhibitors/biosynthesis/physiology; Edema/immunology/metabolism/physiopathology; Endorphins/antagonists & inhibitors/biosynthesis/physiology; Freund's Adjuvant/administration & dosage; Inflammation/immunology/metabolism/physiopathology; Leukocytes/drug effects/metabolism/physiology; Methionine/antagonists & inhibitors/biosynthesis/physiology; Naloxone/administration & dosage; Pain/immunology/pathology/prevention & control; Stress/immunology/metabolism/physiopathology

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.

2003

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