| First Author | Umino Y | Year | 2013 |
| Journal | Invest Ophthalmol Vis Sci | Volume | 54 |
| Issue | 2 | Pages | 1536-43 |
| PubMed ID | 23287790 | Mgi Jnum | J:214570 |
| Mgi Id | MGI:5603275 | Doi | 10.1167/iovs.12-10825 |
| Citation | Umino Y, et al. (2013) Loss of scotopic contrast sensitivity in the optomotor response of diabetic mice. Invest Ophthalmol Vis Sci 54(2):1536-43 |
| abstractText | PURPOSE: Diabetes reduces retinal and visual sensitivity to dim light flashes. However, the impact of diabetes on contrast sensitivity in dim light is unknown. Based on the lowered visual sensitivity previously observed, we hypothesized that contrast sensitivity would similarly be reduced. We therefore examined scotopic contrast sensitivity of the optomotor response in the Ins2(Akita/+) mouse model of type 1 diabetes. METHODS: A longitudinal study of spatial and temporal contrast sensitivity in Ins2(Akita/+) mice and wild-type Ins2(+/+) littermates was conducted. Contrast sensitivity of the optomotor response to rotating gratings of various spatial and temporal frequencies was measured at a dim luminance level (2.6 . 10(-5) cd/m2) known to elicit rod- but not cone-driven responses. RESULTS: An early, progressive loss in scotopic contrast sensitivity was observed in Ins2(Akita/+) mice that was absent from Ins2(+/+) littermate controls. The loss in contrast sensitivity developed over a 3- to 4-month period after the onset of hyperglycemia. Ins2(Akita/+) mice exhibited a nonselective 40% loss in sensitivity to all spatial frequencies and a selective loss in sensitivity to fast but not to slow varying gratings (temporal frequencies > 0.1 Hz or, equivalently, speeds > 3 deg/s). Such losses in sensitivity were prevented by glycemic control with insulin treatment. CONCLUSIONS: An association between a model of type 1 diabetes and scotopic contrast sensitivity of the optomotor response is indicated. Ins2(Akita/+) mice exhibit a uniform loss in optomotor contrast sensitivity to all spatial frequencies that, unexpectedly, can be explained as being secondary to a retinal or central loss in sensitivity to high temporal frequencies. |
