Ethanol activates maxi Ca2+-activated K+ channels of clonal pituitary (GH3) cells

J Membr Biol. 1997 Jun 1;157(3):237-45. doi: 10.1007/pl00005895.


The effect of ethanol on maxi Ca2+-activated K+ channels (BK channels) in GH3 pituitary tumor cells was investigated using single-channel recordings and focusing on intracellular signal transduction. In outside-out patches, ethanol caused a transient concentration-dependent increase of BK-channel activity. 30 mm (1.4 per thousand) ethanol significantly increased mean channel open time and channel open probability by 26.3 +/- 9% and 78.8 +/- 10%, respectively; single-channel current amplitude was not affected by ethanol. The augmenting effect of ethanol was blocked in the presence of protein kinase C (PKC) inhibitors staurosporine, bisindolylmaleimide, and PKC (19-31) pseudosubstrate inhibitor as well as by AMP-PNP (5'-adenylylimidodiphosphate), a nonhydrolyzable ATP-analogue, but not by the phospholipase C blocker U-73122. Phosphatase inhibitors microcystin-LR and okadaic acid promoted the ethanol effect. The blocking effect was released at higher concentrations of ethanol (100 mm) suggesting a second site of action or a competition between blockers and ethanol. Our results suggest that the effect of ethanol on BK-channels is mediated by PKC stimulation and phosphorylation of the channels which increases channel activity and hence may influence action potentials duration and hormone secretion.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / metabolism*
  • Clone Cells
  • Ethanol / pharmacology*
  • Ion Channel Gating / drug effects*
  • Pituitary Gland / metabolism*
  • Potassium Channels / drug effects
  • Potassium Channels / metabolism*
  • Rats
  • Signal Transduction*


  • Potassium Channels
  • Ethanol
  • Calcium