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 KATPchannels has been implicated in mediating the analgesic effects of agents such as morphine. However, systematic studies regarding the effects of KATPactivators on nociception and neuronal excitability are scarce.Results: In this study, we describe the antagonistic effects of KATPactivators 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 KATPactivators can moderately activate KATPin DRG neurons. Because the effects of KATPactivators can be reversed by the KATPblocker glyburide, direct activation of KATPis most likely the underlying mechanism.Conclusion: This systematic study clearly demonstrates that activation of KATPcould have significant modulatory effects on the excitability of sensory neurons and thus on sensory behaviors, such as nociception. KATPactivators can be evaluated clinically for the treatment of pain symptoms. © 2011 Du et al; licensee BioMed Central Ltd.
CITATION STYLE
Du, X., Wang, C., & Zhang, H. (2011). Activation of ATP-sensitive potassium channels antagonize nociceptive behavior and hyperexcitability of DRG neurons from rats. Molecular Pain, 7. https://doi.org/10.1186/1744-8069-7-35
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