Increased Na+ and K+ currents in small mouse dorsal root ganglion neurons after ganglion compression

Fan N, Sikand P, Donnelly DF, Ma C, LaMotte RH. Increased Na+ and K+ currents in small mouse dorsal root ganglion neurons after ganglion compression. J Neurophysiol 106: 211-218, 2011. First published April 27, 2011; doi:10.1152/jn.00065.2011.-We investigated the effects of chronic compression (CCD) of the L3 and L4 dorsal root ganglion (DRG) on pain behavior in the mouse and on the electrophysiological properties of the small-diameter neuronal cell bodies in the intact ganglion. CCD is a model of human radicular pain produced by intraforaminal stenosis and other disorders affecting the DRG, spinal nerve, or root. On days 1, 3, 5, and 7 after the onset of compression, there was a significant decrease from preoperative values in the threshold mechanical force required to elicit a withdrawal of the foot ipsilateral to the CCD (tactile allodynia). Whole cell patch-clamp recordings were obtained, in vitro, from small-sized somata and, for the first time, in the intact DRG. Under current clamp, CCD neurons exhibited a significantly lower rheobase compared with controls. A few CCD but no control neurons exhibited spontaneous action potentials. CCD neurons showed an increase in the density of TTX-resistant and TTX-sensitive Na+ current. CCD neurons also exhibited an enhanced density of voltage-dependent K+ current, due to an increase in delayed rectifier K+ current, without a change in the transient or A current. We conclude that CCD in the mouse produces a model of radicular pain, as we have previously demonstrated in the rat. While the role of enhanced K+ current remains to be elucidated, we speculate that it represents a compensatory neuronal response to reduce ectopic or aberrant levels of neuronal activity produced by the injury.