Loss of SUR1 and Kir6.2 ATP-sensitive potassium channel subunits produces comparable neuronal excitability and morphine antinociception

Neuron-specific loss of SUR1 or Kir6.2 in mouse dorsal root ganglion neurons increases excitability and attenuates morphine antinociception, indicating cooperative KATP channel function.

• Why it matters: It is unclear whether both KATP subunits are required in naive peripheral nociception and for opioid analgesia, despite evidence of distinct expression patterns.
• What they did: In mice, neuron-specific Cre-mediated recombination in SUR1 and Kir6.2 floxed animals was tested with whole-cell patch clamp in DRG and diazoxide-induced potassium flux in cultured DRG.
• The result: Loss of either subunit increased DRG excitability, reduced diazoxide-induced potassium flux, and attenuated morphine antinociception; chronic morphine decreased Kir6.2 RNA in mouse DRG but not spinal cords.