期刊
TRENDS IN NEUROSCIENCES
卷 32, 期 12, 页码 611-618出版社
ELSEVIER SCIENCE LONDON
DOI: 10.1016/j.tins.2009.07.007
关键词
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资金
- NIAMS NIH HHS [R01 AR054635-03, R01 AR054635, R01 AR048821-05, R01 AR048821] Funding Source: Medline
- NINDS NIH HHS [P01 NS053709, R01 NS053880, R01 NS053880-04, P01 NS053709-03] Funding Source: Medline
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 (PKC epsilon) 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.
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