ABSTRACT
The purpose of the present study was to investigate the effects of dexmedetomidine (DEX) on neuropathic pain in the chronic compression of dorsal root ganglion (CCD) rat model and the underlying mechanism. Pain behavioral tests were applied to observe the effects of DEX on mechanical allodynia in Sprague Dawley (SD) rats. Whole cell patch clamp was used to observe the influence of DEX on excitability and hyperpolarization-activated inward current (I) of C- and A-type dorsal root ganglion (DRG) neurons. The results showed that mechanical allodynia of CCD rats was significantly inhibited by DEX (P < 0.05). In C- and A-type DRG neurons from the CCD rats, DEX significantly increased rheobase and after hyperpolarizing potential, as well as decreased I current density. These results suggest that DEX could attenuate the neuropathic pain in the CCD rats, and the mechanism might be related to the depressed I current density and excitability of C- and A-type DRG neurons.