EN
BACKGROUND AND AIMS: Demyelination in the experimental models is followed by successful remyelination. However, remyelination in post-spinal cord injuries is failed and often incomplete. The purpose of the present study is to determine if induction of remyelination could promote axon growth in the total spinal cord injury model of the adult rat. METHODS: Demyelination within the dorsal and ventral funiculi were induced with an intraspinal injection of ethidium bromide (EB) either immediately after transection (single injected group) or twice, immediately after and at 5 days post-transection (double injected group). RESULTS: We observed decrease in total area covered by Iba1- positive macrophage and GFAP-positive astrocyte at the injury epicenter in both single and double EB injected rats at 14 dpl. The number of oligodendrocyte precursor cells (OPCs) significantly increased in adjacent to the transection area at 14 days after injury in both experimental groups and remained elevated for 2 months after injury in double injected rats. The highest area of neurofilamentpositive axons at the injury epicenter and lesion adjacent area was observed in double EB injected animals. Neurofilament-positive axons in these animals were frequently found associated with periaxin, which presumably expressed by myelinating Schwann cells. Remyelination improved the recovery of locomotion and supported serotonergic 5HT fiber growth through the injury site. CONCLUSIONS: Our findings suggest that focal demyelination reduces glial scar formation, induces OPCs recruitment and differentiation, and creates a unique environment, which is permissive for spontaneous axon growth which could be promising in order to achieve functional improvement.