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Journal of Neuroscience, Vol 15, 3662-3666, Copyright © 1995 by Society for Neuroscience

ARTICLE

Swelling-induced chloride currents in neuroblastoma cells are calcium dependent

S Basavappa, V Chartouni, K Kirk, V Prpic, JC Ellory and AW Mangel
Department of Physiology, University of Oxford, United Kingdom.

The effects of osmotic stress on chloride (CI-) currents in the human neuroblastoma cell line CHP-100 were evaluated. Following exposure to hypoosmotic solution, an increase in whole-cell CI- current was observed. This current was blocked by the CI- channel blocker 5-nitro-2- (3-phenylpropylamino)-benzoic acid (NPPB). In cells loaded with the CI- permeability marker 125I, exposure to hypoosmotic solution increased 125I efflux by 197 +/- 14% (n = 41, p < 0.05) over controls. This increase was sensitive to NPPB. Hypoosmotic stress also increased cytosolic calcium levels (Ca2+) in fura-2-loaded cells. Pretreatment with EGTA inhibited the increase in cytosolic Ca2+, 125I efflux, and whole-cell CI- current produced by hypoosmotic solution. Antagonists of N-, L-, and T-type Ca2+ channels did not alter stimulation in 125I efflux or cytosolic Ca2+ levels during osmotic stress. However, omega- conotoxin MVIIC, a P-type Ca2+ channel blocker, inhibited hypoosmotically activated whole-cell CI- currents and increases in cytosolic Ca2+. It is concluded that a Ca(2+)-dependent change in CI- permeability is activated in CHP-100 cells in response to osmotic stress.

This article has been cited by other articles:

				S. Basavappa, S. F. Pedersen, N. K. Jorgensen, J. C. Ellory, and E. K. Hoffmann Swelling-Induced Arachidonic Acid Release via the 85-kDa cPLA2 in Human Neuroblastoma Cells J Neurophysiol, March 1, 1998; 79(3): 1441 - 1449. [Abstract] [Full Text] [PDF]

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