Chronic pancreatitis (CP) is a relatively common disorder, characterized by glandular insufficiency and chronic, often intractable, pain. The mechanism of pain in CP is poorly understood. We have previously developed a model of trinitrobenzene sulphonic acid (TNBS)-induced CP that results in nociceptive sensitization in rats. This study is to examine changes in excitability and alteration of voltage-gated potassium currents of dorsal root ganglia (DRG) neurons innervating the pancreas. CP was induced in adult rats by intraductal injection of TNBS. DRG neurons innervating the pancreas were identified by DiI fluorescence labeling. Whole cell patch-clamp recordings were made from acutely dissociated DRG neurons from control and TNBS treated rats. The pancreas-specific DRG neurons displayed more depolarized resting potentials in TNBS-treated rats than those in controls (P<0.02). Some neurons from the TNBS-treated group exhibited spontaneous firings. TNBS-induced CP also resulted in a dramatic reduction in rheobase (P<0.05) and a significant increase in the number of action potentials evoked at twice rheobase (P<0.05). Under voltage-clamp conditions, neurons from both groups exhibited transient A-type (I_A) and sustained outward rectifier K⁺ currents (I_K). Compared to controls, the average I_A but not the average I_K densities were significantly reduced in TNBS group (P<0.05). The steady-state inactivation curve for I_A was displaced by ~20 mV to more hyperpolarized levels in TNBS group. These data suggest that TNBS-treatment increases the excitability of pancreas-specific DRG neurons by suppressing I_A density, thus identifying for the first time a specific molecular mechanism underlying chronic visceral pain and sensitization in CP.