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S.L. Ball, M.T. Pardue, M.A. McCall, R.G. Gregg, N.S. Peachey; Immunohistochemical Analysis of the Outer Plexiform Layer in the Nob Mouse . Invest. Ophthalmol. Vis. Sci. 2003;44(13):1865.
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© ARVO (1962-2015); The Authors (2016-present)
Purpose: : In nob (no-b-wave) mice, a mutation in the gene that encodes for the nyctalopin protein results in a defect in communication between photoreceptors and depolarizing bipolar cells (DBCs). As the role of the nyctalopin protein is unknown, we investigated possible effects of this mutation on the distribution of proteins that are necessary for DBC activation or the generation of a b-wave. Methods: Adult normal and nob mice were enucleated, and the eyes were immersion fixed in 4% paraformaldehyde for 10 min, cryoprotected, embedded and sectioned on a cryostat at 10 µm. Immunohistochemistry reactions were performed using standard protocols with antibodies to the following proteins: PKC, PSD-95, the α1F subunit of voltage gated calcium channels, mGluR6, G0α, bassoon, trkB, and dystrophin. Results:In control retinas, each antibody showed a labeling pattern in the OPL that was comparable to those previously described for mouse retina. In nob mice, the labeling pattern was comparable to controls. Conclusions: The normal distribution of these OPL synaptic proteins in nob mice leads us to two possible explanations. First, although these proteins are correctly localized, in the absence of nyctalopin one or more may not be functional. Alternatively, the defect associated with nob may involve a novel role for nyctalopin in synaptic transmission or the DBC signal transduction cascade.
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