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Neuron. 2012 Oct 18;76(2):370-82. doi: 10.1016/j.neuron.2012.07.029. Epub 2012 Oct 17.

Calcium feedback to cGMP synthesis strongly attenuates single-photon responses driven by long rhodopsin lifetimes.

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1
Center for Neuroscience, University of California, Davis, Davis, CA 95618, USA.

Erratum in

  • Neuron. 2013 Jun 5;78(5):949.

Abstract

Rod photoreceptors generate amplified, reproducible responses to single photons via a G protein signaling cascade. Surprisingly, genetic perturbations that dramatically alter the deactivation of the principal signal amplifier, the GPCR rhodopsin (R∗), do not much alter the amplitude of single-photon responses (SPRs). These same perturbations, when crossed into a line lacking calcium feedback regulation of cGMP synthesis, produced much larger alterations in SPR amplitudes. Analysis of SPRs from rods with and without feedback reveal that the consequences of trial-to-trial fluctuations in R∗ lifetime in normal rods are also dampened by feedback regulation of cGMP synthesis. Thus, calcium feedback trumps the mechanisms of R∗ deactivation in determining the SPR amplitude, attenuating responses arising from longer R∗ lifetimes to a greater extent than those arising from shorter ones. As a result, rod SPRs achieve a more stereotyped amplitude, a characteristic considered important for reliable transmission through the visual system.

PMID:
23083739
PMCID:
PMC3594095
DOI:
10.1016/j.neuron.2012.07.029
[Indexed for MEDLINE]
Free PMC Article
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