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In addition to a fast activating and immediately inactivating inward sodium current, many types of excitable cells possess a noninactivating or slowly inactivating component: the persistent sodium current ( I NaP  ). The  I NaP   is found in normal primary sensory neurons where it is mediated by tetrodotoxin-sensitive sodium channels. The dorsal root ganglion (DRG) is the gateway for ectopic impulses that originate in pathological pain signals from the periphery. However, the role of I NaP  in DRG neurons remains unclear, particularly in neuropathic pain states. Using  in vivo  recordings from single medium- and large-diameter fibers isolated from the compressed DRG in Sprague-Dawley rats, we show that local application of riluzole, which blocks the  I NaP  , also inhibits the spontaneous activity of A-type DRG neurons in a dose-dependent manner. Significantly, riluzole also abolished subthreshold membrane potential oscillations (SMPOs), although DRG neurons still responded to intracellular current injection with a single full-sized spike. In addition, the  I NaP   was enhanced in medium- and large-sized neurons of the compressed DRG, while bath-applied riluzole significantly inhibited the  I NaP   without affecting the transient sodium current ( I NaT  ). Taken together, these results demonstrate for the first time that the  I NaP   blocker riluzole selectively inhibits I NaP  and thereby blocks SMPOs and the ectopic spontaneous activity of injured A-type DRG neurons. This suggests that the  I NaP   of DRG neurons is a potential target for treating neuropathic pain at the peripheral level.

Blockade of Persistent Sodium Currents Contributes to the Riluzole-Induced Inhibition of Spontaneous Activity and Oscillations in Injured DRG Neurons