title: Mechanism of blue-light-induced plasma-membrane depolarization in etiolated cucumber hypocotyls.
abstract: A large, transient depolarization of the plasma membrane precedes the rapid blue-light (BL)-induced growth suppression in etiolated seedlings of Cucumis sativus L.  The mechanism of this voltage transient was investigated by applying inhibitors of ion channels and the plasma-membrane H(+)-ATPase, by manipulating extracellular ion concentrations, and by measuring cell input resistance and ATP levels.  The depolarizing phase was not affected by Ca(2+)-channel blockers (verapamil, La3+) or by reducing extracellular free Ca2+ by treatment with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid (EGTA).  However, these treatments did reduce the rate of repolarization, indicating an inward movement of Ca2+ is involved.  No effects of the K(+)-channel blocker tetraethylammonium (TEA+) were detected.  Vanadate and KCN, used to inhibit the H(+)-ATPase, reduced or completely inhibited the BL-induced depolarization.  Levels of ATP increased by 11-26% after 1-2 min of BL.  Input resistance of trichrome cells, measured with double-barreled microelectrodes, remained constant during the onset of the depolarization but decreased as the membrane voltage became more positive than -90 mV.  The results indicate that the depolarization mechanism initially involves inactivation of the H(+)-ATPase with subsequent transient activation of one or more types of ion channels.
authors.affiliation: Department of Biology, Pennsylvania State University, University Park 16802, USA.
authors.forename: E P
authors.initials: EP
authors.lastname: Spalding
authors.forename: D J
authors.initials: DJ
authors.lastname: Cosgrove
mesh_terms: D000255:Adenosine Triphosphate / Q000032:analysis / Q000502:physiology; D002462:Cell Membrane / Q000201:enzymology / Q000502:physiology / Q000648:ultrastructure; D018553:Cucumis sativus / Q000166:cytology / Q000502:physiology* / Q000528:radiation effects; D004533:Egtazic Acid / Q000494:pharmacology; D004789:Enzyme Activation; D018546:Hypocotyl / Q000502:physiology* / Q000528:radiation effects / Q000648:ultrastructure; D007473:Ion Channels / Q000037:antagonists & inhibitors / Q000502:physiology*; D008027:Light; D008564:Membrane Potentials / Q000502:physiology; D026902:Potassium Channel Blockers; D006180:Proton-Translocating ATPases / Q000037:antagonists & inhibitors / Q000502:physiology*; D019789:Tetraethylammonium; D013757:Tetraethylammonium Compounds / Q000494:pharmacology; D014638:Vanadates / Q000494:pharmacology; D014700:Verapamil / Q000494:pharmacology
chemical_list: D007473:Ion Channels; D026902:Potassium Channel Blockers; D013757:Tetraethylammonium Compounds; D014638:Vanadates; D004533:Egtazic Acid; D019789:Tetraethylammonium; D000255:Adenosine Triphosphate; D014700:Verapamil; D006180:Proton-Translocating ATPases