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R.G. Gregg, P.D. Lukasiewicz, N.S. Peachey, B.T. Sagdullaev, M.A. McCall; Nyctalopin Is Required for Signaling Through Depolarizing Bipolar Cells in the Murine Retina . Invest. Ophthalmol. Vis. Sci. 2003;44(13):4180.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: The nob mouse mutant, which lacks nyctalopin, has no b-wave. We investigated whether this defect was attributed to the inability of depolarizing bipolar cells (DBCs) to respond to glutamate. To determine whether glutamate release from photoreceptors was compromised, visual response properties of nob retinal ganglion cells were examined. Methods: Whole cell recordings from bipolar cells were made in retinal slices from adult normal and nob mice. Current responses to puffs of glutamate were obtained under voltage clamp conditions. Each bipolar cell was filled with Lucifer yellow and classified by its morphology and the laminar location of its cell body and axon terminals. Ganglion cell recordings were made in vivo from the optic nerve, using tungsten electrodes. Computer driven visual stimuli were used to characterize their response properties. Results: In retinas from normal mice, glutamate puffs produced a robust outward current in DBCs and an inward current in hyperpolarizing bipolar cells (HBCs). By contrast, in nob retinas, only HBCs responded to glutamate. The inability to respond to glutamate suggests the nob defect resides in the DBCs. In normal mice, visual responses from ON and OFF center ganglion cells were recorded in similar proportions. In nob retinas only OFF center cells responded to light stimulation. Conclusion: These data indicate nyctalopin is required for modulation by glutamate of the cation current in DBCs and visual processing through the ON pathway.
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