Fig. 6

Axons degeneration of retinal ganglion cells (RGCs) following retinal ischemia/reperfusion (RI/R) triggered a synaptic compensatory response between bipolar cells and RGCs. In the normal condition, RGCs transmit the visual signals to lateral geniculate nucleus (LGN) and superior colliculus (SC) through optic nerve. This function will be weakened following the RI/R induced RGCs’ axons degeneration. In this scenario, bipolar cells strenuously synapse with RGCs to maintain, even recovery the visual function, through up-regulating synaptic vehicle proteins and enhancement of exocytosis. However, no response with post-synaptic elements occurred between bipolar cells and RGCs, which suggests that the mature synapses cannot be formed in this case. Even worse, the increased synaptic vehicle proteins and presynaptic vesicles might induce excitotoxic neurotransmitters release and excessive energy consumption. This may enhance the excitotoxic injury and increase the bipolar cells’ susceptibility to the RI/R