| First Author | Ueno S | Year | 2005 |
| Journal | Exp Eye Res | Volume | 81 |
| Issue | 6 | Pages | 751-8 |
| PubMed ID | 16005871 | Mgi Jnum | J:104250 |
| Mgi Id | MGI:3611591 | Doi | 10.1016/j.exer.2005.04.013 |
| Citation | Ueno S, et al. (2005) Physiological function of S-cone system is not enhanced in rd7 mice. Exp Eye Res 81(6):751-8 |
| abstractText | The rd7mouse is a mutant mouse with a relatively late development of retinal degeneration. Earlier studies have shown that rd7 mice have a distinctive pattern of retinal dysplasia with an increased number of cone cells, particularly those with S (short wavelength)-opsin immunoreactivity. These alterations of the rd7 retina are caused by a mutation in the photoreceptor cell-specific nuclear receptor gene, Nr2e3, which is involved in the signaling pathway regulating photoreceptor cell differentiation, cell maintenance, and cell-cell interactions. The purpose of this study was to determine the physiological properties of the rd7 retina using electroretinographic (ERG) techniques. We found that the maximal a-wave amplitude of the ERG in rd7 mice was already reduced to half of the congenic controls at 6 weeks of age with normal phototransduction sensitivity. The photopic ERGs of rd7 mice were not supernormal, and the amplitudes of the S-cone ERGs were not significantly different from those recorded in controls. These results suggested that even though the number of cones expressing S-opsin is increased, the physiological function of the S-cone system is not enhanced in rd7 mice. |
