The role of ERK activation in the neuronal excitability in the chronically compressed dorsal root ganglia.

We examined the roles of phosphorylation of extracellular signal-regulated protein kinases (pERK) in regulating the excitability of neurons in the dorsal root ganglion (DRG) after chronic compression. A chronic compression of DRG (CCD) induced a significant increase in pERK in intact L4/L5 DRGs of rats as assessed by Western blot analysis. The treatment of U0126, the mitogen-activated protein kinase (MAPK) kinase 1/2 inhibitor, suppressed excitability in CCD-injured DRG neurons but not in naïve DRG neurons. Furthermore, the inhibition of ERK signaling increased A-type fast inactivating potassium current. Taken together, the excitation of CCD neurons might be attributed to the CCD-induced activation of ERK, which suppressed the A-type fast inactivating potassium conductance in CCD neurons.