Peripheral and central mechanisms of inflammatory pain, with emphasis on MAP kinases.
Tissue injury is associated with inflammation and produces inflammatory pain. In animal models, inflammatory pain is normally produced by injection of irritative chemicals into the hindpaw or joint of animal. Inflammatory pain manifests as an expression of neuronal plasticity, which consists of peripheral sensitization (increased sensitivity of primary sensory neurons in the peripheral nervous system, PNS) and central sensitization (increased sensitivity of spinal dorsal horn and other neurons in the central nervous system, CNS). Activation of several protein kinases causes both forms of sensitization via posttranslational, translational, and transcriptional regulation. In particular, mitogen-activated protein kinase (MAPK), such as ERK and p38, is activated by inflammatory mediators in primary sensory and secondary order dorsal horn neurons and participates in the generation and maintenance of inflammatory pain. Development of specific MAPK inhibitors will open a new avenue to the pharmacological intervention of inflammatory pain.
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