By B. L. Kidd1 and L. A. Urban
One of the cardinal features of inflammatory states is that normally innocuous stimuli produce pain. Since the publication of the Melzack–Wall gate control theory in 1965,45 it has been widely appreciated that the nervous system exhibits a range of responses according to different conditions (‘neural plasticity’). Subsequent research has characterized the mechanisms by which these changes occur and highlighted the importance of environmental factors on perception of pain.
This review focuses on key peripheral mechanisms that result in the hypersensitivity state that accompanies inflammation. Recent studies are described which characterize a series of receptors, ion channels and transmitters involved in inflammatory pain. The mechanisms by which inflammatory mediators interact with neurones to produce hypersensitivity are also explored.
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