Abstract
Our recent study has suggested that sodium channel 1.6 (NaV1.6) played a critical role in the generation of high-frequency/bursting discharges in dorsal root ganglion (DRG) neurons and in the development of chronic pain following DRG inflammation or peripheral nerve injury. It has been reported that, in some neurons, resurgent currents mediated by NaV1.6 depend on pore block by the interacting sodium channel β4 (NaVβ4) subunit. In the present study, we injected the rat L4 and L5 dorsal root ganglia (DRGs) with small interfering RNAs directed against NaVβ4 (or a nontargetting control siRNA) in a rat model of low back pain by locally inflaming the L4 and/or L5 DRGs.
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