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F. Jammoul, P. Gondouin, J. Dugardin, D. Pain, R. Caplette, M. Simonutti, C. Craft, S. José-Alain, S. Picaud; Taurine Supplementation Prevents Cone and Retinal Ganglion Cell Damages in Young Vigabatrin-Treated Rats. Invest. Ophthalmol. Vis. Sci. 2009;50(13):3605.
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Vigabatrin (VGB), an antiepileptic drug, induces irreversible visual field constriction and is still widely administered in infantile spasms and as co-treatment in refractory epilepsy. Recently, we found that cone damage was due to a taurine deficiency in adult VGB-treated rats (Jammoul et al., Annals of Neurology, 2008). However, in children treated for infantile spasms, an optic atrophy was also reported. In this study, we therefore investigated the lesions in young VGB-treated rats with a specific emphasis on retinal ganglion cells.
Wistar rats were daily injected with VGB (0.6mg) from 4 to 29 days. Treatments were achieved on the following 3 animal groups: control (I), VGB-treated rats (II) and rats receiving VGB and taurine (5 mg) daily injections (III).
Photopic electroretinogram were statistically significant decreased in VGB-treated animals (group II) as compared to the control group (p<0,001). Taurine supplementation prevented this ERG amplitude decrease (group III). As in adult animals, retinal lesions included cone cell damage, retinal dysplasia with disorganization of the photoreceptor nuclear layer, glial cell reaction. Again, taurine supplementation prevented this retinal lesion. When retinal ganglion cells were quantified on retinal section following their immunostaining with a Brn3A antibody, we observed a 57% cell loss (p<0,001). Taurine supplementation partially prevented this retinal ganglion cell loss (20%).
These results are consistent with our previous study showing that retinal damage is due to a taurine deficiency. It shows further that this taurine deficiency induces both cone and retinal ganglion cell damage. It therefore suggests that taurine supplementation should be considered in VGB treatment for infantile spasms or epilepsy.
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