On the gating mechanisms of the light-dependent conductance in Pecten hyperpolarizing photoreceptors : does light remove inactivation in voltage-dependent K channels?


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dc.contributor.author Gomez, Maria del Pilar
dc.contributor.author Nasi, Enrico
dc.date.accessioned 2008-05-16T15:06:00Z
dc.date.available 2008-05-16T15:06:00Z
dc.date.issued 2005-04-11
dc.identifier.citation Journal of General Physiology 125 (2005): 455-464 en
dc.identifier.uri http://hdl.handle.net/1912/2231
dc.description © 2005 Gomez et al. This article is distributed under the terms of the Creative Commons Attribution-Noncommercial-Share Alike 3.0 Unported License. The definitive version was published in Journal of General Physiology 125 (2005): 455-464, doi:10.1085/jgp.200509269. en
dc.description.abstract The hyperpolarizing receptor potential of ciliary photoreceptors of scallop and other mollusks is mediated by a cGMP-activated K conductance; these cells also express a transient potassium current triggered by depolarization. During steady illumination, the outward currents elicited by voltage steps lose their decay kinetics. One interesting conjecture that has been proposed is that the currents triggered by light and by depolarization are mediated by the same population of channels, and that illumination evokes the receptor potential by removing their steady-state inactivation. Exploiting the information that has become available on the phototransduction cascade of ciliary photoreceptors, we demonstrated that the same downstream signaling elements are implicated in the modulation of voltage-elicited currents: direct chemical stimulation both at the level of the G protein and of the final messenger that controls the light-dependent channels (cGMP) also attenuate the falling phase of the voltage-activated current. Application of a protein kinase G antagonist was ineffective, suggesting that a cGMP-initiated phosphorylation step is not implicated. To ascertain the commonality of ionic pathways we used pharmacological blockers. Although millimolar 4-aminopyridine (4-AP) suppressed both currents, at micromolar concentrations only the photocurrent was blocked. Conversely, barium completely and reversibly antagonized the transient voltage-activated current with no detectable effect on the light-evoked current. These results rule out that the same ionic pores mediate both currents; the mechanism of light modulation of the depolarization-evoked K current was elucidated as a time-dependent increase in the light-sensitive conductance that is superimposed on the inactivating K current. en
dc.description.sponsorship Supported by National Institutes of Health grant EY07559 en
dc.format.mimetype application/pdf
dc.language.iso en_US en
dc.publisher Rockefeller University Press en
dc.relation.uri http://dx.doi.org/10.1085/jgp.200509269
dc.rights.uri http://creativecommons.org/licenses/by-nc-sa/3.0/ *
dc.subject Photoreceptors en
dc.subject CNG channel en
dc.subject Potassium ion channels en
dc.subject Gating, ion channels en
dc.subject Blockers, potassium channel en
dc.title On the gating mechanisms of the light-dependent conductance in Pecten hyperpolarizing photoreceptors : does light remove inactivation in voltage-dependent K channels? en
dc.type Article en
dc.identifier.doi 10.1085/jgp.200509269

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