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Background  Nociceptive responses to noxious stimuli are initiated at peripheral nociceptor terminals. Ion channels play a vital role in pain signal initiation and conduction. Activation of K ATP  channels has been implicated in mediating the analgesic effects of agents such as morphine. However, systematic studies regarding the effects of K ATP  activators on nociception and neuronal excitability are scarce.    Results  In this study, we describe the antagonistic effects of K ATP  activators pinacidil and diazoxide on nocifensive behavior induced by bradykinin (BK), thermo and mechanical stimuli, and the bradykinin-induced hyperexcitability of DRG neurons. We also found that K ATP  activators can moderately activate K ATP  in DRG neurons. Because the effects of K ATP  activators can be reversed by the K ATP  blocker glyburide, direct activation of K ATP  is most likely the underlying mechanism.    Conclusion  This systematic study clearly demonstrates that activation of K ATP  could have significant modulatory effects on the excitability of sensory neurons and thus on sensory behaviors, such as nociception. K ATP  activators can be evaluated clinically for the treatment of pain symptoms.

Activation of ATP-Sensitive Potassium Channels Antagonize Nociceptive Behavior and Hyperexcitability of DRG Neurons from Rats