PMID: 9435186Jan 22, 1998Paper

Ethanol increases the activity of Ca(++)-dependent K+ (mslo) channels: functional interaction with cytosolic Ca++

The Journal of Pharmacology and Experimental Therapeutics
A M DopicoS N Treistman

Abstract

Ethanol (EtOH) reversibly activates large conductance, Ca(++)-activated K+ (BK) channels in rat neurohypophysial terminals, an effect that probably contributes to the inhibition of vasopressin release by this drug. Heterogeneity in the terminal channel population makes it difficult to determine the mechanisms underlying this activation. Here, we report the effects of EtOH on the steady-state activity of BK channels cloned from mouse brain (mslo, alpha subunit) and expressed in Xenopus oocytes. EtOH reversibly increased mslo channel activity in excised patches, showing a potency (EC50 = 24 mM) similar to that reported using native channels. EtOH activation was observed under conditions that make it highly improbable that it is mediated by freely diffusible second messengers, or secondary to G-protein modulation. Rather, it probably results from a functional interaction between the drug and the channel alpha subunit. Activation occurred without increase in the number of functional channels present in the patch and resulted from actions that were a function of EtOH concentration: at < or = 10 mM, activation was due to a decrease in the channel mean closed time, whereas between 25 and 100 mM, activation was due to both a decrease i...Continue Reading

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