Noninvasive alternating current stimulation can induce vision restoration in patients with chronic optic nerve damage and results in electroencephalogram (EEG) aftereffects. To better understand the mechanisms of action, we studied such EEG "aftereffects" of transcorneal alternating current stimulation (tACS) at the chronic posttraumatic state in rats. EEG baseline was recorded from visual cortex under ketamine/xylazine narcosis of healthy rats and rats with chronic severe optic nerve crush. One week later, both groups were again anesthetized and stimulated transcorneally twice for 12 min each time. tACS-induced changes were compared with baseline EEG. Over the course of 65 min narcosis baseline EEG revealed a shift from a dominant delta power to theta. This shift was significantly delayed in lesioned animals compared with healthy controls. tACS applied during the late narcosis stage in normal rats led to significantly increased theta power with a parallel shift of the dominating peak to higher frequency which outlasted the stimulation period by 15 min (aftereffects). EEG in lesioned rats was not significantly changed. In rodents, tACS can induce neuroplasticity as shown by EEG aftereffects that outlast the stimulation period. But this requires a minimal level of brain activation because aftereffects are not seen when tACS is applied during deep anesthesia and not when applied to animals after severe optic nerve damage. We conclude that tACS is only effective to induce cortical plasticity when the the retina can be excited.