May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Modeling Arrestin Translocation in Rod Photoreceptors
Author Affiliations & Notes
  • O. Gross
    Center for Neuroscience, University of California, Davis, Davis, CA
  • M.E. Burns
    Center for Neuroscience, University of California, Davis, Davis, CA
  • Footnotes
    Commercial Relationships  O. Gross, None; M.E. Burns, None.
  • Footnotes
    Support  NEI Grant EY14047
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3743. doi:
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      O. Gross, M.E. Burns; Modeling Arrestin Translocation in Rod Photoreceptors . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3743.

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      © ARVO (1962-2015); The Authors (2016-present)

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Purpose: : Arrestin is localized at high concentrations in the inner segment (IS) of dark adapted rods. During prolonged exposure to light, most of the arrestin moves to the rod outer segment (OS). Similarly, translocation of arrestin back to the IS can be induced by returning the cells to the dark. Arrestin translocation has been reported to be energy–independent, suggesting passive diffusion as a primary mechanism. Translocating arrestin has also been reported to be suprastoichiometric to activated rhodopsin under certain bleaching conditions, suggesting a more complex translocation scheme. Mathematical modeling of arrestin translocation will help to constrain consideration of the so far unknown mechanisms and consequences of this process.

Methods: : Arrestin translocation from IS to OS in response to light was modeled assuming the existence of low affinity IS binding sites and a relatively high binding affinity for activated rhodopsin in the OS. The spatial and temporal distribution of arrestin was plotted under varying conditions, simulating either passive diffusion or active transport. A light–dependent translocation signal was implemented by treating the equilibrium level of free and bound arrestin in the IS as a function of the amount of bleached rhodopsin.

Results: : In simulation, mass translocation (> 50%) of arrestin could be induced by bleach levels of only a few percent when rapid diffusion was coupled with a light–dependent translocation signal. At slightly lower bleach levels, the number of translocating arrestin molecules was proportional to the amount of activated rhodopsin, due to the linearity of the translocation signal at low bleach levels. The total amount of translocating arrestin for partial bleaches was limited by the molar ratio of arrestin to rhodopsin.

Conclusions: : These results provide a set of predictions about the kinetics of plausible arrestin translocation schemes. Paired with single cell electrophysiological recordings, our results will help to identify the mechanisms of arrestin translocation and quantify the consequences of this process for rod signaling.

Keywords: computational modeling • photoreceptors • signal transduction 

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