Fig. 4. Enhanced growth of lesioned corticospinal tract axons in LIF-grafted animals. Nissl stains (A, B) show the relative amounts of host gray matter and white matter in sections close to those pictured in C–F. A, LIF-grafted subject; B, control-grafted subject.dwm, Dorsal white matter; gm, gray matter; vwm, ventral white matter. Arrowsindicate host/graft (g) interface.Inset in A demonstrates that these sections are sampled from regions lateral to the midline; thus, dorsal white matter containing the CST (red ininset) is no longer visible in these sections. WGA-HRP-labeled sections (C–F) demonstrate substantially augmented growth of WGA-HRP-labeled CST axons up to the host/graft interface in host gray matter ventral to the lesion site in LIF-grafted (C, E) but not in control-grafted (D, F) animals. The preponderance of this growth is located in the more dorsally located gray matter rather than in ventrally located gray matter. In dark-field illumination (C, D), the borders between dorsal white matter (dvm), gray matter (gm), and ventral white matter (vwm) can be readily distinguished (indicated bydashed lines). Linear arrays of CST axons of the sort present in the gray matter of these lesioned spinal cords (E, F) are detectable only after injury; normally, CST-labeled ramifications in the gray matter exhibit numerous arborizations of fine, varicose axons but not linear growth. Scale bars: A, B, 220 μm; C, D, 172 μm;E, F, 42 μm.