Ethanol Activates Maxi Ca2+-activated K+ Channels of Clonal Pituitary (GH3) Cells (original) (raw)

Abstract.

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‰) 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.

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Authors and Affiliations

  1. Department of Physiology, Institute of Zoology, University of Salzburg, Hellbrunnerstr. 34, A-5020 Salzburg, Austria, , , , , , AT
    M. Jakab, T.M. Weiger & A. Hermann

Authors

  1. M. Jakab
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  2. T.M. Weiger
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  3. A. Hermann
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Received: 24 July 1996/Revised: 27 December 1996

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Jakab, M., Weiger, T. & Hermann, A. Ethanol Activates Maxi Ca2+-activated K+ Channels of Clonal Pituitary (GH3) Cells .J. Membrane Biol. 157, 237 –245 (1997). https://doi.org/10.1007/PL00005895

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