title: Variation in rhodopsin kinase expression alters the dim flash response shut off and the light adaptation in rod photoreceptors.
abstract: OBJECTIVE
  Rod photoreceptors are exquisitely sensitive light detectors that function in dim light. The timely inactivation of their light responses is critical for the ability of rods to reliably detect and count photons. A key step in the inactivation of the rod transduction is the phosphorylation of the rod visual pigment, rhodopsin, catalyzed by G-protein-dependent receptor kinase 1 (GRK1). Absence of GRK1 greatly prolongs the photoreceptors' light response and enhances their susceptibility to degeneration. This study examined the light responses from mouse rods expressing various levels of GRK1 to evaluate how their function is modulated by rhodopsin inactivation.
  
  
  METHODS
  Transretinal and single-cell rod electrophysiological recordings were obtained from several strains of mice expressing GRK1 at 0.3- to 3-fold the wild-type levels. The effect of GRK1 expression level on the function of mouse rods was examined in darkness and during background adaptation.
  
  
  RESULTS
  Altering the expression of GRK1 from 0.3- to 3-fold that in wild-type rods had little effect on the single photon response amplitude. Notably, increasing the expression level of GRK1 accelerated the dim flash response shut off but had no effect on the saturated response shut off. Additionally, GRK1 excess abolished the acceleration of saturated responses shut off during light adaptation.
  
  
  CONCLUSIONS
  These results demonstrate that rhodopsin inactivation can modulate the kinetics of recovery from dim light stimulation. More importantly, the ratio of rhodopsin kinase to its modulator recoverin appears critical for the proper adaptation of rods and the acceleration of their response shut off in background light.
authors.affiliation: Department of Ophthalmology and Visual Sciences, Washington University School of Medicine, St. Louis, Missouri, USA.
authors.forename: Keisuke
authors.initials: K
authors.lastname: Sakurai
authors.forename: Joyce E
authors.initials: JE
authors.lastname: Young
authors.forename: Vladimir J
authors.initials: VJ
authors.lastname: Kefalov
authors.forename: Shahrokh C
authors.initials: SC
authors.lastname: Khani
mesh_terms: D000221:Adaptation, Ocular / Q000502:physiology*; D000818:Animals; D003623:Dark Adaptation / Q000502:physiology; D051606:G-Protein-Coupled Receptor Kinase 1 / Q000096:biosynthesis / Q000235:genetics*; D005786:Gene Expression Regulation; D005838:Genotype; D055537:Light Signal Transduction / Q000502:physiology*; D051379:Mice; D008822:Mice, Transgenic; D010775:Photic Stimulation; D012313:RNA / Q000235:genetics*; D017948:Retinal Rod Photoreceptor Cells / Q000502:physiology*; D020133:Reverse Transcriptase Polymerase Chain Reaction
chemical_list: D012313:RNA; D051606:G-Protein-Coupled Receptor Kinase 1; C496762:Grk1 protein, mouse