The transition from acute to chronic pain states might be the most important challenge in research to improve clinical treatment of debilitating pain.
We describe a recently identified mechanism of neuronal plasticity in primary afferent nociceptive nerve fibers (nociceptors) by which an acute inflammatory insult or environmental stressor can trigger long-lasting hypersensitivity of nociceptors to inflammatory cytokines.
This phenomenon, "hyperalgesic priming," depends on:
• The epsilon isoform of protein kinase C (PKCvarepsilon)
• And a switch in intracellular signaling pathways that mediate cytokine-induced nociceptor hyperexcitability.
We discuss the impact of this discovery on our understanding of, and ultimately our ability to treat, a variety of enigmatic and debilitating pain conditions, including those associated with repetitive injury, and generalized pain conditions, such as fibromyalgia.
Source: Trends in Neuroscience, Sep 23, 2009. PMID: 19781793, by Reichling DB, Levine JD. Department of Medicine, Division of Rheumatology, and Department of Oral and Maxillofacial Surgery and Division of Neuroscience, University of California, San Francisco, California, USA.