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. 2003;120(1):219-26.
doi: 10.1016/s0306-4522(03)00267-7.

Transient attenuation of protein kinase Cepsilon can terminate a chronic hyperalgesic state in the rat

C A Parada  1 , J J Yeh, D B Reichling, J D Levine
Affiliations

Transient attenuation of protein kinase Cepsilon can terminate a chronic hyperalgesic state in the rat

C A Parada et al. Neuroscience. 2003.

Abstract

Recently we demonstrated that a single 3-day episode of carrageenan-induced acute cutaneous inflammation can create a chronic state of increased susceptibility to inflammatory hyperalgesia. In this latent "primed" state, although there is no ongoing hyperalgesia, the hyperalgesic response to subsequent challenges with inflammatory agent (prostaglandin E2; PGE2) is greatly enhanced. Furthermore, the PGE2-induced hyperalgesia in primed skin was found to require activity of the epsilon isozyme of protein kinase C (PKCepsilon), a second messenger that is not required for PGE2-induced hyperalgesia in control animals. In the present study we tested the hypothesis that activity of PKCepsilon not only plays a critical role in the expression of primed PGE2-induced hyperalgesia, but also in the development and maintenance of the primed state itself. Antisense oligodeoxynucleotide was employed to produce a decrease in PKCepsilon in the nerve, verified by Western blot analysis. PKCepsilon was found to be essential both for the development of carrageenan-induced hyperalgesic priming, as well as for the maintenance of the primed state. Furthermore, hyperalgesic priming could be induced by an agonist of PKCepsilon (pseudo-receptor octapeptide for activated PKCepsilon) at a dose that itself causes no hyperalgesia. The finding that transient inhibition of PKCepsilon can not only prevent the development of priming, but can also terminate a fully developed state of priming suggests the possibility that selective targeting PKCepsilon might be an effective new strategy in the treatment of chronic inflammatory pain.

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