May 2006
Volume 47, Issue 13
ARVO Annual Meeting Abstract  |   May 2006
Functional Comparisons Of Rod And Cone Arrestins In Rod Photoreceptors
Author Affiliations & Notes
  • W.W. Rubin
    Center for Neuroscience, University of California, Davis, Davis, CA
  • J. Chen
    Department of Cell & Neurobiology, Keck School of Medicine, University of Southern California, Los Angeles, CA
  • M.E. Burns
    Center for Neuroscience, University of California, Davis, Davis, CA
  • Footnotes
    Commercial Relationships  W.W. Rubin, None; J. Chen, None; M.E. Burns, None.
  • Footnotes
    Support  NEI Grants EY12576 EY03040 EY14047 EY12155 and the Arnold and Mabel Beckman Macular Research Center and the E. Matilda Ziegler Foundation for the Blind
Investigative Ophthalmology & Visual Science May 2006, Vol.47, 3718. doi:
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      W.W. Rubin, J. Chen, M.E. Burns; Functional Comparisons Of Rod And Cone Arrestins In Rod Photoreceptors . Invest. Ophthalmol. Vis. Sci. 2006;47(13):3718.

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

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Purpose: : Although rods and cones use similar phototransduction cascades, they have distinct response properties, with the less sensitive cones exhibiting faster recovery kinetics. One difference between the cascades of rods and cones is the expression of distinct arrestin genes. In rods, high affinity binding of rod arrestin (ARR1) is required for timely deactivation of phosphorylated, light–activated rhodopsin (R*). In cones, cone arrestin (CAR) is presumed to control cone opsin deactivation, although this has not been shown. We have asked whether the differences in recovery kinetics of rods and cones can be explained in part by the expression of these distinct arrestins.

Methods: : The expression of mouse cone arrestin (mCAR) was directed to rods using the mouse opsin promoter. These mice were subsequently crossed into the rod arrestin knockout (arr1–/–) background. To assay the function of mCAR, suction electrode recordings were performed on single rods from arr1–/– and mCARarr1–/– mice.

Results: : Light responses of arr1–/– and mCARarr1–/– rods were qualitatively similar. The activation phases of the photoresponse were indistinguishable; dim flash responses rose along similar trajectories and had identical times to peak and single photon response amplitudes. Furthermore, measurements of sensitivity were not changed by the expression of mCAR. The recovery phases of arr1–/– and mCARarr1–/– rods were both biphasic: an initial fast phase, lasting hundreds of milliseconds, preceded a much slower phase, lasting dozens of seconds. The time constants of recovery for each phase were similar in arr1–/– and mCARarr1–/– rods. There were significant differences, however, in the extent of the initial phase of recovery. At every flash strength tested, the amplitude of the mCARarr1–/– responses after the fast phase of recovery was significantly smaller than that of arr1–/– responses.

Conclusions: : The incomplete rescue of response recovery in mCARarr1–/– rods and the similar time courses of arr1–/– and mCARarr1–/– responses indicates that cone arrestin cannot fully quench the activity of R*. However, the reduced amplitude of the mCARarr1–/– responses during the slow recovery phase suggests that mCAR can lower the rate of transducin activation, which likely reflects a low affinity interaction of mCAR with R*.

Keywords: photoreceptors • electrophysiology: non-clinical • signal transduction 

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