BKCa channels expressed in sensory neurons modulate inflammatory pain in mice

Pain. 2014 Mar;155(3):556-565. doi: 10.1016/j.pain.2013.12.005. Epub 2013 Dec 11.


Large conductance calcium-activated potassium (BKCa) channels are important regulators of neuronal excitability. Although there is electrophysiological evidence for BKCa channel expression in sensory neurons, their in vivo functions in pain processing have not been fully defined. Using a specific antibody, we demonstrate here that BKCa channels are expressed in subpopulations of peptidergic and nonpeptidergic nociceptors. To test a functional association of BKCa channel activity in sensory neurons with particular pain modalities, we generated mice in which BKCa channels are ablated specifically from sensory neurons and analyzed their behavior in various models of pain. Mutant mice showed increased nociceptive behavior in models of persistent inflammatory pain. However, their behavior in models of neuropathic or acute nociceptive pain was normal. Moreover, systemic administration of the BKCa channel opener, NS1619, inhibited persistent inflammatory pain. Our investigations provide in vivo evidence that BKCa channels expressed in sensory neurons exert inhibitory control on sensory input in inflammatory pain states.

Keywords: Conditional knockout mice; Dorsal root ganglion; Inflammatory pain; Large conductance Ca(2+)-activated K(+) channels.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Female
  • Gene Expression Regulation*
  • Inflammation / metabolism
  • Inflammation / pathology
  • Large-Conductance Calcium-Activated Potassium Channel alpha Subunits / biosynthesis*
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Pain / metabolism*
  • Pain / pathology
  • Pain Measurement / methods*
  • Sensory Receptor Cells / metabolism*
  • Sensory Receptor Cells / pathology


  • BKCa protein, mouse
  • Large-Conductance Calcium-Activated Potassium Channel alpha Subunits