Table of Contents
ISRN Ophthalmology
Volume 2013, Article ID 814814, 7 pages
http://dx.doi.org/10.1155/2013/814814
Research Article

Lens Injury Has a Protective Effect on Photoreceptors in the RCS Rat

1Department of Ophthalmology, University of Münster Medical School, Domagkstraße 15, 48149 Münster, Germany
2Centre for Ophthalmology, Experimental Vitreoretinal Surgery, Schleichstraße 12/1, 72076 Tübingen, Germany
3Experimental Neurology, Department of Neurology, Heinrich Heine University, Life Science Centre, Merowingerplatz 1a, D-40225 Düsseldorf, Germany
4Experimental Neurology, University Ulm, Albert-Einstein-Allee 11, 89081 Ulm, Germany

Received 10 June 2013; Accepted 5 August 2013

Academic Editors: M. Nakazawa and Y. F. Shih

Copyright © 2013 Peter Heiduschka et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Lens injury induced activation of retinal glia, and subsequent release of ciliary neurotrophic factor (CNTF) and leukaemia inhibitory factor (LIF) potently protect axotomised retinal ganglion cells from apoptosis and promotes axon regeneration in the injured optic nerve. The goal of the current study was to investigate if similar effects may also be applicable to rescue photoreceptors from degeneration in a model of retinitis pigmentosa. Lens injury was performed in the Royal College of Surgeons (RCS) rats at the age of one month. The survival of photoreceptors was evaluated histologically, and retinal function was analysed by electroretinography (ERG). Expression of CNTF was also analysed. Lens injury significantly enhanced the survival of photoreceptors 1 month after surgery compared to untreated controls, which was associated with an enhanced ERG response. In addition, lens injury significantly protected photoreceptors from degeneration in the contralateral eye, although to a much lesser extent. We could show that lens injury is sufficient to transiently delay the degeneration of photoreceptors in the RCS rat. The observed neuroprotective effects may be at least partially mediated by an upregulation of CNTF expression seen after lens injury.