We anticipate that non-selective COX inhibitor, the selective COX-2 inhibitor, and the selective COX-3 inhibitor will differentially alter prostanoid production over the time course evaluated, and that primary sensory neurons innervating in the inflammatory tissues may differentially express COX isoenzymes that differ in sensitivity to prototypic NSAIDs, coxibs, and acetaminophen. We also anticipate that several SNPs will contribute to the individual differences in COX expression and drug responses, which has implications for individual variation in pain, analgesic responses, and neuronal plasticity.