K+ channels and the microglial respiratory burst

Rajesh Khanna, Lipi Roy, Xiaoping Zhu, Lyanne C. Schlichter

Research output: Contribution to journalArticlepeer-review


Microglial activation following central nervous system damage or disease often culminates in a respiratory that is necessary for antimicrobial function, but, paradoxically, can damage bystander cells. We show that several K+ channels are expressed and play a role in the respiratory burst of cultured rat microglia. Three pharmacologically separable K+ currents had properties of Kv1.3 and the Ca2+/ calmodulin-gated channels, SK2, SK3, and SK4. mRNA was detected for Kv1.3, Kv1.5, SK2, and/or SK3, and SK4. Protein was detected for Kv1.3, Kv1.5, and SK3 (selective SK2 and SK4 antibodies not available). No Kv1.5-like current was detected, and confocal immunofluorescence showed the protein to be subcellular, in contrast to the robust membrane localization of Kv1.3. To determine whether any of these channels play a role in microglial activation, a respiratory burst was stimulated with phorbol 12-myristate 13-acetate and measured using a single cell, fluorescence-based dihydrorhodamine 123 assay. The respiratory burst Was markedly inhibited by blockers of SK2 (apamin) and SK4 channels (clotrimazole and charybdotoxin), and to a lesser extent, by the potent Kv1.3 blocker agitoxin-2.

Original languageEnglish (US)
Pages (from-to)C796-C806
JournalAmerican Journal of Physiology - Cell Physiology
Issue number4 49-4
StatePublished - 2001


  • Calcium-activated potassium channels
  • Kv1.3
  • Microglial activation
  • Reactive oxygen intermediates
  • Small-conductance K channels

ASJC Scopus subject areas

  • Physiology
  • Cell Biology


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