Potentiation of sural nerve Abeta action potential after neurogenic inflammation.

Abstract

Inflammatory mediators modulate voltage-gated sodium channels through protein kinase-mediated pathways. However, it is not clear whether neurogenic inflammation may also alter the properties of distantly located channels along axon shafts supplying the inflamed dermatome. In this study, localized inflammation was induced via intradermal injection of capsaicin within the receptive field of the sural nerve, and compound action potentials (CAP) evoked by sural nerve stimulation were recorded from the sciatic nerve proximally. The area measured under the A beta CAP increased significantly within 5 min after capsaicin injection. Distal injection of lidocaine at the ankle division of the sural nerve prior to capsaicin injection reversed this increase. In addition, application of a lipophilic protein kinase inhibitor H7 (100 microM) through a perfusion chamber placed on the sciatic nerve also reversed this increase. Our results suggest that during neurogenic inflammation, action potential activity is increased, triggering activation of protein kinases that may rapidly alter membrane conductance to potentiate action potential propagation along peripheral nerves.