Hypotonicity and ethanol modulate BK channel activity and chloride currents in GH4/C1 pituitary tumour cells

Authors: Jakab, M.; Schmidt, S.; Grundbichler, M.1; Paulmichl, M.; Hermann, A.2; Weiger, T.2; Ritter, M.1

Source: Acta Physiologica, Volume 187, Numbers 1-2, May/June 2006 , pp. 51-59(9)

Publisher: Wiley-Blackwell

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Abstract Aim: 

Description of the effects of hypotonic cell swelling and ethanol on maxi Ca2+-activated K+ channel (BK channel) activity and Cl channel activity in GH4/C1 pituitary tumour cells. Methods: 

Whole cell-, cell attached- and outside-out patch clamp measurements, fluorescence (fluo-3) measurements of intracellular Ca2+ concentration, cell size video monitoring. Results: 

GH4/C1 pituitary tumour cells respond to both hypotonicity and ethanol with cell swelling which is followed by a regulatory volume decrease (RVD). Tetraethylammonium and 4,4′-diisothiocyanatostilbene-2,2′-disulphonic acid (DIDS) induced cell swelling per se and inhibited hypotonicity induced RVD. Ethanol-induced swelling is paralleled by an increase in the intracellular Ca2+ concentration and augmented by DIDS. BK channel activation by hypotonicity and ethanol is demonstrated in patch clamp experiments both in intact cells (cell attached configuration) and a subset of excised membrane patches (outside-out configuration). Cell swelling and addition of ionomycin under isotonic conditions leads to the activation of outwardly rectifying Cl currents with time dependent activation at positive potentials. Conclusions: 

In GH4/C1 cells both hypotonicity and ethanol lead to cell swelling, RVD and to activation of BK channels. The hypotonicity-induced BK channel activation can also be observed in cell free outside-out patches. Hypotonicity, but not ethanol leads to the activation of Cl channels with features of Ca2+-activated Cl currents.

Keywords: BK channels; GH4/C1 cells; cell volume regulation; chloride channels; ethanol; regulatory volume decrease currents/channels

Document Type: Research Article

DOI: http://dx.doi.org/10.1111/j.1748-1716.2006.01544.x

Affiliations: 1: Institute of Physiology and Pathophysiology, Paracelsus Private Medical University Salzburg, Salzburg, Austria 2: Department of Cell Biology, Division of Animal Physiology, University of Salzburg, Salzburg, Austria

Publication date: May 1, 2006

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