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We hypothesized that abnormal activity and adrenergic sensitivity in injured dorsal root ganglion (DRG) neurons are due to an intrinsic alteration of the cell body membrane. We investigated the effects of adrenergic stimulus on the activities of Ca2+and K+channels of DRG neurons in a rat chronic constriction injury (CCI) model. At first, we demonstrated thermal hyperalgesia and sprouting sympathetic nerve fibers in the ipsilateral L4-L5 DRGs. Using whole-cell patch clamp techniques, we found that α2-adrenergic stimulus by 10 μM norepinephrine (NE) inhibited inward currents (IBa, Ba2+as a charge carrier) through voltage-dependent Ca2+channels (VDCCs) of DRGs in the CCI model by 42%, whereas it enhanced the IBaby 18% in control animals. The inhibitory effect of NE disappeared by pretreatment with the N-type VDCC antagonist ω-conotoxin GVIA (1 μM). NE shifted the inactivation curve to a more negative potential, showing that it has inhibitory effects on IBaboth in activated and in inactivated states. α2-Adrenergic stimulus also inhibited outward K+currents by 24% in the CCI model, while it had no effect on the currents in control animals. The inhibitory effect of NE was blocked by pretreatment with the Ca2+-activated K+(KCa) channel antagonist charybdotoxin (40 nM). The NE-induced inhibitory effects both on N-type VDCC and on KCachannels in injured DRG neurons of the CCI model could lead to cell membrane depolarization, resulting in a spontaneous discharge of action potential and an increase in sensitivity to adrenergic stimulus.