Welcome to the new version of CaltechAUTHORS. Login is currently restricted to library staff. If you notice any issues, please email coda@library.caltech.edu
Published March 15, 2000 | Published
Journal Article Open

Mice Lacking G-Protein Receptor Kinase 1 Have Profoundly Slowed Recovery of Cone-Driven Retinal Responses


G-Protein receptor kinase 1 (GRK1) ("rhodopsin kinase") is necessary for the inactivation of photoactivated rhodopsin, the light receptor of the G-protein transduction cascade of rod photoreceptors. GRK1 has also been reported to be present in retinal cones in which its function is unknown. To examine the role of GRK1 in retinal cone signaling pathways, we measured in mice having null mutations of GRK1 (GRK1 −/−) cone-driven electroretinographic (ERG) responses, including an a-wave component identified as the field potential generated by suppression of the circulating current of the cone photoreceptors. Dark-adapted GRK1 −/− animals generated cone-driven ERGs having saturating amplitudes and sensitivities in both visible and UV spectral regions similar to those of wild-type (WT) mice. However, after exposure to a bright conditioning flash, the cone-driven ERGs of GRK1 −/− animals recovered 30–50 times more slowly than those of WT mice and similarly slower than the cone-driven ERGs of mice homozygously null for arrestin (Arrestin −/−), whose cone (but not rod) response recoveries were found to be as rapid as those of WT. Our observations argue that GRK1 is essential for normal deactivation of murine cone phototransduction and provide the first functional evidence for a major role of a specific GRK in the inactivation of vertebrate cone phototransduction.

Additional Information

© 2000 Society for Neuroscience. Received Sept. 23, 1999; revised Dec. 21, 1999; accepted Dec. 29, 1999. This work was supported by grants from the National Eye Institute.

Attached Files

Published - 2209.full.pdf


Files (331.1 kB)
Name Size Download all
331.1 kB Preview Download

Additional details

August 21, 2023
October 18, 2023