Identifying the mechanisms underlying the early stage of hypoxic injury of the retinocollicular neurotransmission will provide valuable insights that may be beneficial for the future intervening in visual attention and perception deficits and preventing their progressions. Previously, we have demonstrated that the protein kinase C (PKC) signaling pathway mediates hypoxia-induced LTP of NMDA retinocollicular neurotransmission. The potent and selective inhibitor of PKC - chelerythrine chloride (ChC, 5 µM) completely blocked the induction of LTP by hypoxia and even reversed already induced one. Here, we decided to test the role of the PKC in hypoxia-induced temporary suppression of the AMPA retinocollicular transmission.We recorded pharmacologically isolated AMPA neurotransmission in cocultivated pairs of rat retinal ganglion cells and superficial superior colliculus neurons under normoxic and hypoxic conditions, using the paired patch-clamp technique and method of fast local superfusion. Spontaneous activity was recorded in the absence of presynaptic stimulation.We observed that the presence of ChC completely blocked hypoxia-induced suppression of AMPA retinocollicular neurotransmission. We also found that ChC eliminated hypoxia-induced decrease in the occurrence frequency of spontaneous AMPA events. The obtained results reflect that hypoxia-induced suppression of AMPA is mediated by PKC and strengthen the idea that ChC might be a promising agent for the prevention and treatment of hypoxic injuries retinocollicular neurotransmission.