Bradykinin and peripheral sensitization
Haibin Wang, Corina Ehnert, Gary J. Brenner, Clifford J. Woolf
Abstract
Haibin Wang, Corina Ehnert, Gary J. Brenner, Clifford J. Woolf
Abstract
Pain hypersensitivity after tissue injury and inflammation is contributed to by a reduction in the threshold and an increase in the responsiveness of the peripheral terminals of high-threshold nociceptor neurons, the phenomenon of peripheral sensitization. Bradykinin, acting via G-protein-coupled receptors expressed by the sensory neurons, links to multiple intracellular signaling pathways that in turn interact with voltage-gated and ligand-gated ion channels, changing their properties in such a way as to enhance the response to peripheral stimuli.
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Pain hypersensitivity after tissue injury and inflammation is contributed to by a reduction in the threshold and an increase in the responsiveness of the peripheral terminals of high-threshold nociceptor neurons, the phenomenon of peripheral sensitization. Bradykinin, acting via G-protein-coupled receptors expressed by the sensory neurons, links to multiple intracellular signaling pathways that in turn interact with voltage-gated and ligand-gated ion channels, changing their properties in such a way as to enhance the response to peripheral stimuli.
Key concepts: Sensitization, Nociceptor, Bradykinin, Peripheral, Intracellular, Chemistry, Receptor, Neuroscience