RT Journal Article
SR Electronic
T1 Swelling-induced chloride currents in neuroblastoma cells are calcium dependent
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 3662
OP 3666
DO 10.1523/JNEUROSCI.15-05-03662.1995
VO 15
IS 5
A1 S Basavappa
A1 V Chartouni
A1 K Kirk
A1 V Prpic
A1 JC Ellory
A1 AW Mangel
YR 1995
UL http://www.jneurosci.org/content/15/5/3662.abstract
AB 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.