Loose ligation of the rat sciatic nerve is accompanied by changes in the subcellular content of protein kinase C beta II and gamma in the spinal dorsal horn.

This study examined whether loose ligation of the sciatic nerve was accompanied by specific changes in protein kinase C (PKC) betaII and gamma isozymes in the spinal dorsal horn. The isozyme staining pattern was visualized with immunocytochemistry. Their content in subcellular fractions was estimated from Western immunoblots. In control animals, PKC betaII immunoreactivity extended from lamina I into lamina III, while PKC gamma immunoreactivity was concentrated within laminae II and III. In ligated animals exhibiting thermal hyperalgesia, the content of both PKC betaII and gamma in the synaptosomal membrane fraction, but not crude cytosolic fraction, was significantly greater by an average of 40% from their respective controls. These data support suggestions that peripheral nerve injury engenders plastic changes in the dorsal horn to contribute to the development of persistent pain.