Abstract:

A rat model of acute high intraocular pressure was established by injecting saline into the anterior chamber of the left eye. Synaptophysin expression was increased in the inner plexiform layer at   2 hours following injury, and was widely distributed in the outer plexiform layer at 3–7 days, and then decreased to the normal level at 14 days. This suggests that expression of this presynaptic functional protein experienced spatiotemporal alterations after elevation of intraocular pressure. There was no significant change in the fluorescence intensity and distribution pattern for synapse-associated protein 102 following elevated intraocular pressure. Synapse-associated protein 102 immunoreactivity was confined to the outer plexiform layer, while synaptophysin immunoreactivity spread into the outer plexiform layer and the outer nuclear layer at 3 and 7 days following injury. These alterations in presynaptic elements were not accompanied by changes in postsynaptic components.

Key words: synaptophysin, synapse-associated protein 102, synaptic plasticity, elevated intraocular pressure, retina, neural regeneration