Enhanced cone dysfunction in rats homozygous for the P23H rhodopsin mutation

• Published in: Neuroscience letters Vol. 382; no. 1; pp. 16 - 21
• Main Authors: Pinilla, I., Lund, R.D., Sauvé, Y.
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 01.07.2005; Elsevier
• Subjects: Aging - physiology; Animals; Animals, Genetically Modified; Biological and medical sciences; Cones; Electroretinogram; Electroretinography; Flicker; Flicker Fusion; Fundamental and applied biological sciences. Psychology; Homozygote; Male; Medical sciences; Mutation - physiology; Ophthalmology; P23H; Rat; Rats; Rats, Sprague-Dawley; Retina - growth & development; Retinal Cone Photoreceptor Cells - physiology; Retinal Degeneration - physiopathology; Retinal Rod Photoreceptor Cells - physiology; Retinitis pigmentosa; Retinopathies; Rhodopsin - genetics; Rhodopsin - physiology; Vertebrates: nervous system and sense organs; P23H; Rat; Cones; Retinitis pigmentosa; Electroretinogram; Flicker; Electroretinography; Rhodopsin; Retinopathy; Cone; Rodentia; Electrophysiology; Genetic disease; Eye disease; Vertebrata; Mammalia; Animal; Mutation

The heterozygous P23H transgenic rat is a model of autosomal dominant retinitis pigmentosa, in which a mutation in the rhodopsin gene leads to a rapid loss of rods and a more protracted loss of cones. It has been suggested that rods play an essential role in preserving cones. We tested this hypothes...