Intracellular Mg2+ enhances the function of BK-type Ca2+-activated K+ channels

J. Shi, J. Cui

Research output: Contribution to journalArticlepeer-review

100 Scopus citations


BK channels modulate neurotransmitter release due to their activation by voltage and Ca2+. Intracellular Mg2+ also modulates BK channels in multiple ways with opposite effects on channel function. Previous single-channel studies have shown that Mg2+ blocks the pore of BK channels in a voltage-dependent manner. We have confirmed this result by studying macroscopic currents of the mslol channel. We find that Mg2+ activates mslol BK channels independently of Ca2+ and voltage by preferentially binding to their open conformation. The mslo3 channel, which lacks Ca2+ binding sites in the tail, is not activated by Mg2+. However, coexpression of the mslol core and mslo3 tail produces channels with Mg2+ sensitMty similar to mslol channels, indicating that Mg2+ sites differ from Ca2+ sites. We discovered that Mg2+ also binds to Ca2+ sites and competitively inhibits Ca2+-dependent activation. Quantitative computation of these effects reveals that the overall effect of Mg2+ under physiological conditions is to enhance BK channel function.

Original languageEnglish
Pages (from-to)589-605
Number of pages17
JournalJournal of General Physiology
Issue number5
StatePublished - 2001


  • BK channel
  • Calcium
  • Competitive inhibition
  • Ion channel gating
  • Magnesium


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