Crush and transection of the optic nerve damages retinal ganglion cells, leading to apoptotic cell death.
1 2 4 14 Many attempts have been made to rescue the retinal ganglion cells from cell death by various methods—among them, inhibition of apoptotic pathways, the administration of neurotrophic factors, implantation of Schwann cells.
14 In addition, several studies have demonstrated an enhancement of retinal axon regeneration.
14 Transcorneal stimulation, as used in the present experiments, has also been reported to protect retinal ganglion cells against cell death after optic nerve transection.
5 However, the present results could not be explained by the protective effect against retinal ganglion cell death, as described earlier. The death of retinal ganglion cells is minimal during the first week and the number of those cells significantly decreases between 2 and 4 weeks after the injury.
1 2 4 14 In contrast, in the present experiments, the optic nerve crush immediately exerts a deleterious effect on the VEP, and the electrical stimulation given just after the crush restores the VEP amplitude rapidly within hours. Such a rapid improvement in the VEP cannot be explained by inhibition of retinal ganglion cell death, which has a much slower time course. Furthermore, it is highly unlikely that degenerated axons regenerated and restored the functional innervations during the electrical stimulation for 6 hours. The rapid decrease in VEP amplitude after the optic nerve crush may reflect a block of nerve conduction as reported previously,
15 because the retinal functions estimated by ERG remain almost completely intact immediately after an optic nerve injury.
16 The present results, with the previous finding,
5 indicate that electrical stimulation can reverse the acute reduction of VEP amplitude and prohibit the ensuing processes which lead to a permanent impairment of optic nerve function and the retinal ganglion cell death.