Immunohistochemical analysis of the outer plexiform layer in the nob mouse shows no abnormalities

• Published in: Visual neuroscience Vol. 20; no. 3; p. 267
• Main Authors: Ball, Sherry L, Pardue, Machelle T, McCall, Maureen A, Gregg, Ronald G, Peachey, Neal S
• Format: Journal Article
• Language: English
• Published: England 01-05-2003
• Subjects: Animals; Calcium Channels - metabolism; Dendrites - ultrastructure; Disks Large Homolog 4 Protein; Electroretinography; GTP-Binding Protein alpha Subunits, Gi-Go - metabolism; Guanylate Kinases; Immunohistochemistry; Intracellular Signaling Peptides and Proteins; Membrane Proteins; Mice; Mice, Inbred NOD - metabolism; Nerve Tissue Proteins - metabolism; Presynaptic Terminals - metabolism; Receptors, Metabotropic Glutamate - metabolism; Retina - metabolism; Retina - physiopathology; Retinal Rod Photoreceptor Cells - ultrastructure
• ISSN: 0952-5238
• DOI: 10.1017/S0952523803203059

In the nob mouse, a mutation in nyctalopin results in a loss of signal transmission from photoreceptors to depolarizing bipolar cells (DBCs). We used immunohistochemical techniques to assess the expression pattern of proteins found at either the photoreceptor terminal or bipolar cell dendrites within the outer plexiform layer. We labeled normal and nob retinas with antibodies against mGluR6, PKC, G0alpha, bassoon, PSD-95, the alpha1F subunit of voltage-gated calcium channels, trkB, and dystrophin. All labeling patterns in nob and normal retinas were comparable to those previously reported in mouse retina. Our results indicate that the absence of nyctalopin does not disrupt the expression pattern of other proteins known to be required for synaptic transmission.