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

Published online by Cambridge University Press:  23 September 2003

SHERRY L. BALL
Affiliation:
Research Service, Cleveland VA Medical Center, Cleveland Department of Psychology, Case Western Reserve University, Cole Eye Institute, Cleveland Clinic Foundation, Cleveland
MACHELLE T. PARDUE
Affiliation:
Research Service, Atlanta VA Medical Center, Decatur Department of Ophthalmology, Emory University, Atlanta
MAUREEN A. MCCALL
Affiliation:
Department of Ophthalmology and Visual Sciences, University of Louisville, Louisville Department of Psychological and Brain Sciences, University of Louisville, Louisville
RONALD G. GREGG
Affiliation:
Department of Psychological and Brain Sciences, University of Louisville, Louisville Department of Biochemistry and Molecular Biology, University of Louisville, Louisville
NEAL S. PEACHEY
Affiliation:
Research Service, Cleveland VA Medical Center, Cleveland Department of Neurosciences, Case Western Reserve University, Cole Eye Institute, Cleveland Clinic Foundation, Cleveland

Abstract

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, G, bassoon, PSD-95, the α1F 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.

Type
Research Article
Copyright
© 2003 Cambridge University Press

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