Temporal response properties of the primary and secondary rod-signaling pathways in normal and Gnat2 mutant mice.
Multiple signaling pathways have been proposed for rod vision in the mammalian retina. The primary and secondary rod pathways have been characterized in humans with the scotopic 15-Hz flicker electroretinogram (ERG). The purpose of this study was to determine whether the response properties of these pathways in the mouse are similar to those of humans. C57BL/6J and Gnat2(cpfl3) mutant mice lacking functional cones were used in these experiments. Standard ERG recording techniques were employed. Response functions were obtained for a range of flash intensities (-4.7logcd-s/m(2) to -0.2logcd-s/m(2)) and temporal modulation frequencies (1-30Hz). The mouse intensity-response functions to 15-Hz flickering stimuli possessed the same features as that of humans - a local amplitude minimum and a rapid phase change in the intensity region where the primary and secondary pathways are mutually inhibitory. However, the secondary pathway in the mouse did not achieve the same level of sensitivity as previously shown for humans, suggesting inter-species differences in post-receptoral signal processing. In Gnat2(cpfl3) mutant mice, the secondary pathway was completely abolished. Measurements of temporal acuity indicated that the primary and secondary rod pathways could mediate temporal frequencies as high as 30 and 50Hz, respectively. The response functions for mice are similar to those of humans, although the evidence suggests that the primary rod pathway dominates all rod-mediated signal processing in the mouse. Nevertheless, these results demonstrate the feasibility of measuring non-invasively the performance characteristics of the primary and secondary rod retinal pathways in the mouse and provide a mechanism for testing hypotheses about the action of disease where post-receptoral cells are differentially affected.
Nusinowitz
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Jules Stein Eye Institute, UCLA School of Medicine, Los Angeles, CA, USA. nusinowitz@jsei.ucla.edu
Ridder
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Ramirez
J
J
D000818:Animals; D004596:Electroretinography; D005136:Eye Proteins / Q000235:genetics* / Q000502:physiology; D005425:Flicker Fusion / Q000502:physiology; D020962:Heterotrimeric GTP-Binding Proteins / Q000235:genetics* / Q000502:physiology; D051379:Mice; D008810:Mice, Inbred C57BL; D008817:Mice, Mutant Strains; D009154:Mutation; D010775:Photic Stimulation / Q000379:methods; D017949:Retinal Cone Photoreceptor Cells / Q000502:physiology; D017948:Retinal Rod Photoreceptor Cells / Q000502:physiology*; D015398:Signal Transduction / Q000502:physiology; D014795:Visual Pathways / Q000502:physiology
D005136:Eye Proteins; C515337:Gnat2 protein, mouse; D020962:Heterotrimeric GTP-Binding Proteins