Content area
Abstract
Mouse mutants for proteins expressed in the dystrophin-glycoprotein complex at the photoreceptor terminal have electroretinogram (ERG) b-waves with a delayed onset and time course. The b-wave is defined by the sum of PII generated by depolarizing bipolar cells and slow PIII generated by Müller glial cells. In this study, we evaluated the hypothesis that the abnormalities observed in one of these mutants, Large ^sup vls^, are caused by abnormal response properties of slow PIII.
To isolate slow PIII, we crossed the Large ^sup vls^ mutant to a mouse line (Gpr179 ^sup nob5^) that lacks the ERG b-wave but maintains normal photoreceptor function and in which retinal degeneration does not occur. ERGs were recorded to strobe flash stimuli after overnight dark adaptation.
In comparison with control responses, the a-wave and slow PIII had comparable waveforms but were reduced in amplitude in Large ^sup vls^ mice. The magnitude of this reduction was comparable for these components, and across stimulus luminance. There was no stimulus condition where the amplitude of slow PIII was larger than control.
The data obtained are inconsistent with the idea that the b-wave abnormalities noted in Large ^sup vls^ mutant mice are caused by abnormal response properties of slow PIII.[PUBLICATION ABSTRACT]