Agonists of protease‐activated receptor 2 (PAR₂) evoke hyperexcitability of dorsal root ganglia (DRG) neurons by unknown mechanisms. We examined the cellular mechanisms underlying PAR₂‐evoked hyperexcitability of mouse colonic DRG neurons to determine their potential role in pain syndromes such as visceral hyperalgesia. Colonic DRG neurons were identified by injecting Fast Blue and DiI retrograde tracers into the mouse colon. Using immunofluorescence, we found that DiI‐labelled neurons contained PAR₂ immunoreactivity, confirming the presence of receptors on colonic neurons. Whole‐cell current‐clamp recordings of acutely dissociated neurons demonstrated that PAR₂ activation with a brief application (3 min) of PAR₂ agonists, SLIGRL‐NH₂ and trypsin, evoked sustained depolarizations (up to 60 min) which were associated with increased input resistance and a marked reduction in rheobase (50% at 30 min). In voltage clamp, SLIGRL‐NH₂ markedly suppressed delayed rectifier I_K currents (55% at 10 min), but had no effect on the transient I_A current or TTX‐resistant Na⁺ currents. In whole‐cell current‐clamp recordings, the sustained excitability evoked by PAR₂ activation was blocked by the PKC inhibitor, calphostin, and the ERK_1/2 inhibitor PD98059. Studies of ERK_1/2 phosphorylation using confocal microscopy demonstrated that SLIGRL‐NH₂ increased levels of immunoreactive pERK_1/2 in DRG neurons, particularly in proximity to the plasma membrane. Thus, activation of PAR₂ receptors on colonic nociceptive neurons causes sustained hyperexcitability that is related, at least in part, to suppression of delayed rectifier I_K currents. Both PKC and ERK_1/2 mediate the PAR₂‐induced hyperexcitability. These studies describe a novel mechanism of sensitization of colonic nociceptive neurons that may be implicated in conditions of visceral hyperalgesia such as irritable bowel syndrome.