Journal
MOLECULAR AND CELLULAR NEUROSCIENCE
Volume 43, Issue 4, Pages 414-421Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.mcn.2010.01.008
Keywords
Vigabatrin; Retina; Retinal ganglion cell; Epilepsy; Vision
Categories
Funding
- INSERM
- Universite Pierre et Marie Curie (Paris VI)
- Fondation Ophtalmologique A. de Rothschild (Paris)
- Agence Nationale pour la Recherche (ANR GABARET, ANR GLAUCOME)
- Federation des Aveugles de France
- City of Paris
- Regional Council of Ile de France and Lundbeck US (USA)
- University of Tichcrine (Syria)
- NIH [EY015851, EY03040]
- RPB
Ask authors/readers for more resources
The anti-epileptic drug vigabatrin induces an irreversible constriction of the visual field, but is still widely used to treat infantile spasms and some forms of epilepsy. We recently reported that vigabatrin-induced cone damage is due to a taurine deficiency. However, optic atrophy and thus retinal ganglion cell degeneration was also reported in children treated for infantile spasms. We here show in neonatal rats treated from postnatal days 4 to 29 that the vigabatrin treatment triggers not only cone photoreceptor damage, disorganisation of the photoreceptor layer and gliosis but also retinal ganglion cell loss. Furthermore, we demonstrate in these neonatal rats that taurine supplementation partially prevents these retinal lesions and in particular the retinal ganglion cell loss. These results provide the first evidence of retinal ganglion cell neuroprotection by taurine. They further confirm that taurine supplementation should be administered with the vigabatrin treatment for infantile spasms or epilepsy. (C) 2010 Elsevier Inc. All rights reserved.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available