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The retinal toxicity of an antiepileptic drug blocking the GABAtransaminase: GABA excitotoxicity or taurine deficiency? Serge Picaud, Institut de la Vision, Paris By contrast to brain structures, GABA, the main inhibitory neurotransmitter, remains excitatory in the adult retinal network. Furthermore, it can activate GABAc receptors, which do not desensitize and thus generate large sustained responses. These specificities could explain the retinal toxicity of vigabatrin, an anti-epileptic drug. Indeed, this drug blocks the GABA-transaminase and thus increases up to 5 fold the retinal GABA concentration. In patients, it was found to generate an irreversible constriction of the visual field. Despite this major secondary effect, the damaging consequences of seizures and the drug efficacy were such that the vigabatrin (sabril) remains the first line drug for the treatment of infantile spasms and a third line drug for some forms of epilepsy in adults. The presentation will describe our recent work on GABA function at photoreceptor terminals and its implication in photoreceptor toxicity. In particular, we will present how we elucidated the mechanism of vigabatrinelicited photoreceptor toxicity. Finally, we will discuss different strategies to prevent the retinal toxicity of the anti-epileptic drug and future treatments.