Inhibition of M current in sensory neurons by exogenous proteases: a signaling pathway mediating inflammatory nociception.

ABSTRACT: Inflammatory pain is thought to be mediated in part through the action of inflammatory mediators on membrane receptors of peripheral nerve terminals, however, the downstream signaling events which lead to pain are poorly understood. In this study we investigated the nociceptive pathways induced by activation of protease-activated receptor 2 (PAR-2) in damage-sensing (nociceptive) neurons from rat dorsal root ganglion (DRG). We found that activation of PAR-2 in these cells strongly inhibited M-type potassium currents (conducted by Kv7 potassium channels). Such inhibition caused depolarization of the neuronal resting membrane potential leading, ultimately, to nociception. Consistent with this mechanism, injection of the specific M channel blocker XE991 into rat paw induced nociception in a c

SUBMITTER: Linley JE 

PROVIDER: S-EPMC6087463 | biostudies-literature | 2008 Oct

REPOSITORIES: biostudies-literature