Late phase long-term potentiation (LTP) in the CNS requires dendritic protein synthesis. This specialized form of on-demand translation of new proteins is mediated by activity-dependent regulation of translation that requires the movement of mRNAs to dendritic sites. This mode of translation is thought to be dependent on the coordinated action of a number of kinases including aurora, which leads to polyadenylation of poly-A poor mRNAs, and the mammalian target of rapamycin (mTOR) which phosphorylates ribosomal kinases initiating translation. We have tested the hypothesis that these kinases are involved in ongoing nocifensive behaviors in the formalin test in mice. Intrathecal (IT) injection of rapamycin (mTOR inhibitor, 1 and 10ug) inhibited the second phase of the formalin test without affecting the first phase. A maximal inhibition of ~75% was observed at the highest dose of rapamycin. The aurora kinase inhibitor ZM-447439 at 10ug IT also inhibited the second phase of the formalin test by ~75% without affecting the first phase. Using immunohistochemistry with phosphorylation-specific antibodies, we found that, following formalin injection, mTOR and its downstream target ribosomal S6 kinase are located in large neurons of the lamina V, presumably wide dynamic range neurons. These findings indicate that coordinated actions of kinases that regulate translational activity are involved in nocifensive behavior in the second phase of the formalin test in mice. Moreover, they suggest that localized-dendritic translation is required for the full expression of central sensitization following a persistent noxious input.