Taurine Promotes Retinal Ganglion Cell Survival Through GABAB Receptor Activation

Retinal ganglion cell (RGC) degeneration occurs in numerous retinal diseases, either as a primary process like in glaucoma, or secondary to photoreceptor loss and no efficient compound targeting directly RGC neuroprotection is yet available. We previously described that taurine exerts a direct protective effect on RGCs cultured under serum-deprived conditions. Because taurine was known to have an agonist-like activity for GABA/glycine receptors, we investigated here if the taurine-elicited neuroprotective effect may be mediated through the activation of these receptors using selective antagonist ligands. RGCs were purified, seeded in 96-well plate and maintained in culture during 6 days in vitro. Viable cells were labelled with calcein and densities in full-well area were then automatically counted. Here we show that the protective effect of taurine against RGC loss observed under serum deprivation can be mediated through the GABAB receptor stimulation. Hence, two selective agonists, including baclofen, at this metabotropic GABAB receptor were found to reproduce taurine action by enhancing RGC survival in culture. This study suggests that GABAB receptor stimulation provides direct neuroprotection for RGCs. Accordingly, drugs targeting GABAB receptor may represent a new way for the prevention of RGC degeneration.