The ability of regenerated CNS axons to form synapses and conduct neural signals is unclear. This study found that, in mice, deletion of phosphatase and tensin homologue (Pten) and suppressor of cytokine signalling 3 (Socs3) promoted the regeneration of transected retinal ganglion cell (RGC) axons and the reformation of RGC–superior colliculus (SC) synapses. However, these axons were not myelinated, leaving axonal voltage-gated potassium channels (VGKCs) exposed, and preventing functional recovery on an optomotor task. Pharmacological VGKC blockade enabled optogenetic RGC stimulation to induce SC activity and improved optomotor performance. So, remyelination is needed to restore function of regenerated axons.