title: Swelling-induced chloride currents in neuroblastoma cells are calcium dependent.
abstract: 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.
authors.affiliation: Department of Physiology, University of Oxford, United Kingdom.
authors.forename: S
authors.initials: S
authors.lastname: Basavappa
authors.forename: V
authors.initials: V
authors.lastname: Chartouni
authors.forename: K
authors.initials: K
authors.lastname: Kirk
authors.forename: V
authors.initials: V
authors.lastname: Prpic
authors.forename: J C
authors.initials: JC
authors.lastname: Ellory
authors.forename: A W
authors.initials: AW
authors.lastname: Mangel
mesh_terms: D017609:Barium Compounds / Q000494:pharmacology; D002118:Calcium / Q000378:metabolism*; D002121:Calcium Channel Blockers / Q000494:pharmacology; D002462:Cell Membrane / Q000187:drug effects / Q000502:physiology; D018118:Chloride Channels / Q000037:antagonists & inhibitors / Q000502:physiology*; D002712:Chlorides / Q000378:metabolism* / Q000494:pharmacology; D003600:Cytosol / Q000378:metabolism; D004110:Diltiazem / Q000494:pharmacology; D004533:Egtazic Acid / Q000494:pharmacology; D006801:Humans; D007038:Hypotonic Solutions / Q000494:pharmacology; D007454:Iodides / Q000378:metabolism; D007700:Kinetics; D008564:Membrane Potentials / Q000187:drug effects / Q000502:physiology; D008978:Mollusk Venoms / Q000494:pharmacology; D009447:Neuroblastoma; D009532:Nickel / Q000494:pharmacology; D009579:Nitrobenzoates / Q000494:pharmacology*; D018408:Patch-Clamp Techniques; D010455:Peptides / Q000494:pharmacology; D012965:Sodium Chloride; D013997:Time Factors; D014407:Tumor Cells, Cultured; D020866:omega-Conotoxin GVIA; D020960:omega-Conotoxins
chemical_list: D017609:Barium Compounds; D002121:Calcium Channel Blockers; D018118:Chloride Channels; D002712:Chlorides; D007038:Hypotonic Solutions; D007454:Iodides; D008978:Mollusk Venoms; D009579:Nitrobenzoates; D010455:Peptides; D020960:omega-Conotoxins; C024986:barium chloride; C075851:omega-conotoxin-MVIIC; C058176:5-nitro-2-(3-phenylpropylamino)benzoic acid; D012965:Sodium Chloride; D004533:Egtazic Acid; D009532:Nickel; D020866:omega-Conotoxin GVIA; D004110:Diltiazem; D002118:Calcium