Abstract
AbstractPurpose The P23H rhodopsin mutation is an extensively studied model of ADRP. We evaluated the anatomical changes using SD‐OCT and correlate the findings and retinal thickness values with immunocytochemistry. Functional changes were analyzedMethods Heterozygous P23H pigmented transgenic rats aged from P18 to P180 were studied. LE rats bred with Sprague Dawley (SD) 1 month old served as wild type controls. Visual acuity and contrast sensitivity evaluation was performed every month. Corneal ERGs were recorded under scotopic and photopic conditions. Retinal thicknesses at different levels (total thickness, ONL + RPE, ONL and IPL), fundus autofluorescence (FAF) and fluorescein angiography was performed in 3 animals at P150 using Spectralis OCT and HRA (Heidelberg Engineering, Germany). Retinas were immunostained for ICC.Results Retinal thicknesses diminution was seen in OCT sections, with a clear loss of ONL and morphological modifications. Statically differences were found between groups in all evaluated thicknesses. In the P23H rats, change in FAF was noted comparing to control group, as sparse autofluorescent dots. No relevant changes were observed in the angiography pattern. ICC showed a progressive decrease in ONL thickness. Functional changes were progressive with time.Conclusion Anatomical changes in pigmented P23H can be observed using SD‐OCT and immunocytochemistry, with a good correlation between their values. SD‐OCT and FAF are important tools for research in retinal degenerations.
Highlights
Mutations in the rhodopsin gene are a common cause of retinitis pigmentosa (RP),1 with P23H being one of the most common autosomal mutations of this gene (Dryja et al, 1990), and accounting for approximately one third of RP cases in the USA (Dryja et al, 2000)
Pigmented rats are easier to use for visual acuity evaluation with the optomotor system and to define the lines of the Optical coherence tomography (OCT) exploration
Their visual acuity resolution is higher than that of albino rats, which helps to distinguish the effect of the degeneration from the result of any therapeutic approach that we use on them
Summary
Mutations in the rhodopsin gene are a common cause of retinitis pigmentosa (RP), with P23H being one of the most common autosomal mutations of this gene (Dryja et al, 1990), and accounting for approximately one third of RP cases in the USA (Dryja et al, 2000). 1www.sph.uth.tmc.edu/RetNet/disease.htm have been examined, at both anatomical and electrophysiological level (Machida et al, 2000; Cuenca et al, 2004; Pinilla et al, 2005), using the P23H transgenic rat (Lewin et al, 1998). These studies have relied on animals bred with an albino background, which is likely to increase the complexity of the retinal degenerative process. The pigmented background makes it easier to use functional evaluation tests for visual features such as visual acuity and contrast sensitivity
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
