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Gwen M. Sturgill-Short, Neal S. Peachey; Abnormal Slow PIII Component Does Not Account For The Abnormal ERG b-waves Of LargeVls Mice. Invest. Ophthalmol. Vis. Sci. 2012;53(14):2459.
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© ARVO (1962-2015); The Authors (2016-present)
Mouse mutants for Large, fukutin and other proteins that glycosylate α-dystroglycan have abnormal ERGs in which the b-wave has a delayed onset, reduced amplitude and slow kinetics. As the b-wave is derived from the interaction of PII and slow PIII, reflecting activity of depolarizing bipolar cells (DBCs) and Müller cells, respectively, this ERG phenotype could reflect a change in the response properties of PII or slow PIII. To evaluate the possibility that the slow PIII component is abnormal in these models, we crossed the Largevls allele to a no b-wave mouse mutant background, and evaluated the response properties of slow PIII in dark-adapted ERG recordings.
To generate study mice, we crossed the Largevls allele to a nob5 background. Mice were examined at 1 month of age. After overnight dark-adaptation, ERGs were recorded from anesthetized animals to strobe flash stimuli. ERG components generated by photoreceptors (a-wave) and Müller cells (slow PIII) were analyzed across a ~5 log unit range of stimulus luminance.
The overall waveform of Largevls/vls/nob5 mutant mice was not different from that of Largevls/+/nob5 or Large+/+/nob5 littermates. Both the a-wave and slow PIII components were reduced in amplitude in Largevls/vls/nob5 mutant mice. The magnitude of this reduction was equivalent for these two response measures.
These results indicate that the abnormal b-waves noted in Largevls/vls mutant mice cannot be attributed to a change in slow PIII response properties. A similar conclusion is likely to apply to other mouse mutants with similar b-wave abnormalities.
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