Light-induced Potassium Research Articles

Light-induced potassium desorption from polydimethylsiloxane film

Potassium photoejection from polydimethylsiloxane surfaces has been observed and analyzed in detail. By diode laser absorption spectroscopy the K concentration in a sealed measurement cell without buffer gas has been monitored as a function of the environment variables, like temperature, flooding light wavelength and power. The dynamic evolution of the process has been measured too, showing differences compared to previous measurements with different alkali-metal atoms. Saturation spectroscopy on the K D1 line has been performed at room temperature by taking advantage of this phenomenon. PACS. 34.50.Dy Interactions of atoms and molecules with surfaces; photon and electron emission; neu- tralization of ions - 42.50.Ct Quantum description of interaction of light and matter; related experiments - 68.43.Tj Photon stimulated desorption

Evidence for a distinct light-induced calcium-dependent potassium current in Hermissenda crassicornis.

A model of phototransduction is developed as a first step toward a model for investigating the critical interaction of light and turbulence stimuli within the type B photoreceptor of Hermissenda crassicronis. The model includes equations describing phototransduction, release of calcium from intracellular stores, and other calcium regulatory mechanisms, as well as equations describing ligand-gating of a rhabdomeric sodium current. The model is used to determine the sources of calcium in the soma, whether calcium or IP3 is a plausible ligand of the light-induced sodium current, and whether the light-induced potassium current is equivalent to the calcium-dependent potassium current activated by light-induced calcium release. Simulations show that the early light-induced calcium elevation is due to influx through voltage-dependent channels, whereas the later calcium elevation is due to release from intracellular stores. Simulations suggest that the ligand of the fast, light-induced sodium current is IP3 but that there is a smaller, prolonged component of the light-induced sodium current that is activated by calcium. In the model, the calcium-dependent potassium current, located in the soma, is activated only slightly by light-induced calcium elevation, leading to the prediction that a calcium-dependent potassium current, active at resting potential, is located in the rhabdomere and is responsible for the light-induced potassium current.

The influence of MgCl 2 and APB on the light-induced potassium changes and the ERG b-wave of the isolated superfused rat retina

The ERG and the extracellular potassium concentration, [K +] 0, of the isolated superfused rat retina were measured in a physiological solution and in solutions containing 10 mM MgCl 2 or 100 μM APB. MgCl 2 nearly abolished the b-wave, but the light-induced distal [K +] 0 increase was enlarged from 0.13 ± 0.05 to 0.28 ± 0.08 mM. There was also an increase in the light-induced [K +] 0 in the proximal retina. APB abolished the b-wave completely, and the distal light-induced [K +] 0 increase was then replaced by a [K +] 0 decrease. Upon return to the control solution, there was a larger transitory [K +] 0 increase than under control conditions, and this occurred before the b-wave had returned. Under these experimental conditions, the distal [K +] 0 increase could not be correlated with the b-wave, and so the Müller cells are unlikely to be the main source of the rising phase of the b-wave. More probable sources of the b-wave are the on-bipolar cells with their metabotropic and ionotropic receptors, with only the latter apparently being blocked by MgCl 2. The extracellular [K +] 0 changes, however, had an influence upon the slow potentials of the ERG.

The c-wave of the electroretinogram possesses a third component from the proximal retina

ERG and light-induced extracellular potassium ([K +] o) changes have been measured in isolated retinas of both Rana esculenta and Rana temporaria. The conditions of the preparations have been varied. Isolated frog retinas kept receptor side-upward in a moist chamber without perfusion showed the well-known slow PIII in the ERG. Retinas superfused from the receptor side, with O 2 enrichment at their vitreal surface, however, exhibit a slow cornea-positive potential in the ERG. The slow ERG-potentials relate to different light-induced potassium changes in the proximal retina. There was a long lasting and larger proximal potassium increase in adequately maintained retinas but a smaller and shorter one in preparations lacking superfusion and oxygen. There was no significant difference between the size of potassium decrease around receptors of retinas supervised from their vitreal side and those supervised from receptor side. A reduction of slow PIII should therefore not be responsible for the slow cornea-positive potential. The long lasting and larger (by 59%) potassium increase in the proximal retina may counteract the potential in the Mu¨ller cells caused by the potassium decrease around receptors and thereby cancel slow PIII and generate a third component of the electroretinogram c-wave.

The neural retina of the frog contributes a slow cornea-positive potential to the electroretinogram.

A c-wave-like cornea-positive potential in the isolated rabbit retina has been described. In this study, frog retinas were investigated to see if the neural retina contributes a slow cornea-positive component to the c-wave of the electroretinogram. The eye cups of both Rana esculenta and Rana temporaria exhibited a normal electroretinogram with c-wave, a larger proximal light-induced extracellular potassium increase, a small distal extracellular potassium increase and an extracellular potassium decrease around photoreceptors. Isolated frog retinas kept receptor side-upward in a moist chamber without perfusion showed the well-known slow PIII generated by the potassium decrease around receptors. If the isolated retinas were well perfused, the slow PIII was not seen, but a cornea-positive d.c. potential sometimes appeared after the b-wave. The different slow potentials seemed to relate to different light-induced potassium changes in the proximal retina. There was a long-lasting proximal potassium increase in the superfused retinas but a quick return of the proximal potassium increase to the baseline in the retinas lacking oxygen at the vitreal side. The lasting proximal potassium increase in adequately maintained retinas may counteract the potassium decrease around receptors and cancel slow PIII.

Light-induced potassium fluxes in the skate retina

Changes in the extracellular concentration of potassium [K +] o in response to photic stimulation were studied in the skate retina with the aid of ion-selective electrodes. The results confirm earlier studies in demonstrating that the light-evoked changes originate at three intraretinal sites; an efflux of K + was recorded in the regions of the two plexiform (synaptic) layers, whereas a decrease in [K +] o occurred in the extracellular space surrounding the photoreceptors. Prolonged illumination induced long-term alterations in the levels of [K +] o which, depending upon the retinal depth of the recording electrode, contained contributions from the various sinks and sources of [K +] o. In addition, the marked undershoot of the baseline level of [K +] o that followed termination of the stimulus suggested the activity of a metabolically driven process for the uptake of extracellular potassium.

Ion transport induced by light and antibiotics IN CHROMATOPHORES FROM Rhodospirillum rubrum.

On illumination, chromatophores of Rhodospirillum rubrum took up hydrogen ions from the medium. Hydrogen ion uptake was inhibited or reversed by uncoupling agents and by Triton‐X114. Addition of valinomycin in the dark to chromatophores suspended in a medium of low KCl concentration gave rise to a loss of potassium ion from the chromatophores, and a slow H+‐uptake. Illumination gave rise to a further efflux of potassium ion, and a stimulated H+‐uptake. The light‐induced potassium ion efflux increased in extent with increasing external KCl concentration. At high KCl concentrations hydrogen ion efflux occurred on addition of valinomycin in the dark, and a greatly stimulated initial rate of H+‐uptake on illumination was observed. Addition of gramicidin to chromatophores in the dark gave rise to effects similar to those observed with valinomycin. On illumination, the uptake of hydrogen ion was somewhat inhibited, and rapidly reversed in the dark. Addition of nigericin in the dark to chromatophores suspended in a medium of low KCl concentration gave rise to a rapid efflux of potassium ion, and an uptake of hydrogen ion which was nearly stoichiometric in rate and extent. On illumination an inhibited H+‐uptake occurred, together with an uptake of potassium ion from the medium. The inhibition of H+‐uptake, and the extent of K+‐uptake were dependent on nigericin concentration and KCl concentration. The sum of the extent of K+‐uptake and the extent of H+‐uptake was approximately the same in all cases, indicating that an exchange of hydrogen ion within the chromatophores for potassium ion in the medium had occurred. Nigericin gave rise to hydrogen ion efflux from chromatophores suspended in media of high KCl concentration when added in the dark or light. The efflux observed in the light was more extensive and represented a reversal of hydrogen ion uptake. The KCl concentration at which nigericin caused no pH change was shifted from about 4 mM in the dark to about 0.4 mM in the light. The pH gradient across the chromatophore membrane was calculated to be approximately 1 pH unit. Valinomycin inhibited nigericin induced K+‐uptake in the light. At high KCl concentrations nigericin inhibited H+‐uptake in the absence or presence of valinomycin. No marked inhibition of photophosphorylation by nigericin or valinomycin alone was observed even at high KCl concentrations. However, when both antibiotics were present together in the reaction medium, inhibition was observed which was dependent on the KCl concentration. In the absence of added KCl, no inhibition occured but at 10 mM KCl phosphorylation was 86%, and at 100 mM, 93% inhibited. Similar results were obtained when phosphorylation was coupled to electron flow in uninhibited chromatophores, or through N‐methyl phenazonium methosulphate in 2‐heptyl‐4‐hydroxy quinoline N‐oxide inhibited chromatophores.Similar effects were observed when dianemycin was used instead of nigericin. The mechanism of action of the antibiotics tested is discussed. It is suggested that their mode of action on chromatophore membranes is the same as that shown for artificial membrane systems. In particular, it is proposed that nigericin and dianemycin are able to catalyse a cation/cation or cation/hydrogen ion exchange across lipid barriers, which is closely coupled and electrically neutral.

Light-induced potassium efflux from spinach chloroplasts

Light-induced potassium efflux from spinach chloroplasts