Pain-related increases in spinal cord membrane-bound protein kinase C following peripheral nerve injury.
Neuropathic pain following nerve injury is thought to involve central nervous system Ca(2+)-mediated neuronal plastic changes. This study provides evidence that induction and/or maintenance of post-injury neuropathic pain behaviors in the rat is associated with increases in membrane-bound protein kinase C (PKC), a Ca(2+)-dependent process known to mediate central nervous system neuronal plasticity. In addition, spinal cord administration of GM1 ganglioside, an intracellular inhibitor of PKC translocation/activation, reverses both increased levels of membrane-bound PKC and pain-related behaviors. Thus, persistent post-injury neuropathic pain may be mediated by the initiation of excitatory neuropathological processes resulting from an increase in membrane-bound PKC.
Mao
J
J
Department of Physiology, Medical College of Virginia, Virginia Commonwealth University, Richmond 23298.
Price
D D
DD
Mayer
D J
DJ
Hayes
R L
RL
D000818:Animals; D001522:Behavior, Animal / Q000187:drug effects; D005677:G(M1) Ganglioside / Q000494:pharmacology; D010146:Pain / Q000201:enzymology*; D059348:Peripheral Nerve Injuries; D015240:Phorbol 12,13-Dibutyrate / Q000494:pharmacology; D011493:Protein Kinase C / Q000378:metabolism*; D051381:Rats; D013116:Spinal Cord / Q000201:enzymology*
D015240:Phorbol 12,13-Dibutyrate; D005677:G(M1) Ganglioside; D011493:Protein Kinase C