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Controlling Pain by Influencing Neurogenic Pathways

Authors
Journal
Rheumatic Disease Clinics of North America
0889-857X
Publisher
Elsevier
Publication Date
Volume
31
Issue
1
Identifiers
DOI: 10.1016/j.rdc.2004.09.001
Disciplines
  • Pharmacology

Abstract

Neurogenic inflammation and ensuing pain can be modulated by inhibiting the function of primary afferent neurons. The best studied mechanism to accomplish such inhibition is the opioid system. Under inflammatory conditions, the anterograde axonal transport of opioid receptors from dorsal root ganglia toward the peripheral sensory nerve endings is augmented. The increased number of opioid receptors (among other mechanisms) leads to improved analgesic effects of exogenously administered ligands (eg, morphine) and of endogenous leukocyte-derived opioid peptides (eg, β-endorphin). A current concept proposes that during inflammatory processes endogenous opioid peptides can be secreted from immunocytes, occupy peripheral opioid receptors on sensory nerve endings, and produce analgesia by inhibiting the excitability of these nerves or the release of proinflammatory neuropeptides. This article focuses on the role of peripheral opioid receptors in pain control and on novel pharmaceutical concepts for the treatment of patients who suffer from rheumatoid arthritis and other inflammatory pain.

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