Enhancing axonal regeneration and sprouting may be a strategy to promote functional recovery after neural injuries. To set up a partial injury model in the mouse visual system for the functional assessment, we induced the glaucomatous neuropathy by injecting silicone oil (SO) intracamerally into mice. This strategy mechanically obstructed aqueous flow and elevated the intraocular pressure (IOP). Stress imposed by the sustained intraocular hypertension lead to the progressive axonal degeneration and the apoptotic death of retinal ganglion cells (RGCs). We found that RGCs were extensively depleted as soon as one week after injury, with SMI32-positive alpha RGCs being more sensitive to this type of injury than TBR2-positive RGCs. In consistence with the degeneration of RGCs, we o...[ Read more ]

Enhancing axonal regeneration and sprouting may be a strategy to promote functional recovery after neural injuries. To set up a partial injury model in the mouse visual system for the functional assessment, we induced the glaucomatous neuropathy by injecting silicone oil (SO) intracamerally into mice. This strategy mechanically obstructed aqueous flow and elevated the intraocular pressure (IOP). Stress imposed by the sustained intraocular hypertension lead to the progressive axonal degeneration and the apoptotic death of retinal ganglion cells (RGCs). We found that RGCs were extensively depleted as soon as one week after injury, with SMI32-positive alpha RGCs being more sensitive to this type of injury than TBR2-positive RGCs. In consistence with the degeneration of RGCs, we observed functional deficits in two weeks after injury. We also found continuous RGC loss even after silicone oil was removed to reinstate IOP, suggesting a lagged cell death. This partial injury model may help our future work on evaluating regenerative strategies for neural repair.