FIGURE 6.

Electron micrographs demonstrating the prevention of myelination or axon loss and inhibition of neuronal apoptosis by CNTF and C16 treatment. (A,B) Normal control group [(A), normal myelinated axons exhibited dark ring-shaped myelin sheaths surrounding the axon; (B), normal nuclei of neuron with uncondensed chromatin]. (C–F) Vehicle-treated EAE rats at week 2 post-immunization. The myelin sheath displayed splitting, vacuoles (showed by arrow), and loose and fused changes, and axons were shrunken and dissolving (C). Severe leaking out of the blood vessels and tissue emeda were detected in the extracellular space surrounding the vessels [showed by arrow in (D)]. (E) Infiltrated leukocytes (showed by arrow) near the vascular endothelial cell (showed by red arrowhead). (F) The neurons of the vehicle control showed apoptotic signs of shrunken nuclei with condensed, fragmented, and marginated nuclear chromatin. The CNTF- (G), C16- (H), and C16+CNTF-treated (I) groups exhibited more lightly vacuolated myelin sheaths. The neighboring nuclei (J) of C16+CNTF-treated rats resembled the normal ultrastructure. At week 8 post-immunization in the vehicle control group, demylination (arrow) and remyelination (arrowhead) simultaneously appeared in vehicle-treated EAE rats (K). Meanwhile, more remyelinated fibers appeared in C16+CNTF-treated (L) groups.