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Retinal ganglion cells (RGCs) consume large quantities of energy to convert light information into a neuronal signal, which makes them highly susceptible to hypoxic injury. This study aimed to investigate the potential protection by baclofen, a GABA B  receptor agonist of RGCs against hypoxia-induced apoptosis. Cobalt chloride (CoCl 2 ) was applied to mimic hypoxia. Primary rat RGCs were subjected to CoCl 2  with or without baclofen treatment, and RNA interference techniques were used to knock down the GABA B 2 gene in the primary RGCs. The viability and apoptosis of RGCs were assessed using cell viability and terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assays, Hoechst staining, and flow cytometry. The expression of cleaved caspase-3, bcl-2, bax, Akt, phospho-Akt, protein kinase RNA (PKR)-like ER kinase (PERK), phospho-PERK, eIF2α, phospho-eIF2α, ATF-4 and CCAAT/enhancer-binding protein homologous protein (CHOP) were measured using western blotting. GABA B 2 mRNA expression was determined using quantitative real-time polymerase chain reaction (qRT-PCR) analysis. Our study revealed that CoCl 2  significantly induced RGC apoptosis and that baclofen reversed these effects. CoCl 2 -induced reduction of Akt activity was also reversed by baclofen. Baclofen prevented the activation of the PERK pathway and the increase in CHOP expression induced by CoCl 2 . Knockdown of GABA B 2 and the inactivation of the Akt pathway by inhibitors reduced the protective effect of baclofen on CoCl 2 -treated RGCs. Taken together, these results demonstrate that baclofen protects RGCs from CoCl 2 -induced apoptosis by increasing Akt activity and by suppressing the PERK pathway and CHOP activation.

Baclofen Protects Primary Rat Retinal Ganglion Cells from Chemical Hypoxia-Induced Apoptosis Through the Akt and PERK Pathways