FIG. 2. BDA-labeling of CST originating from the contralesional intact hemisphere.

A. A representative coronal section showing BDA injection and injury cavity. B: A representative transverse section showing the BDA-labeled CST in the ventral-most part of the dorsal funiculus (white asterisk, also applicable to D–F and H–J). C: Simplified schematic illustration of TBI, BDA injection, and CST. Unilateral TBI causes cortical injury which affects the CST (dotted lines). BDA was injected into the contralesional intact cortex (stereotaxic coordinates: 1 and 2 mm posterior to the bregma, 3 and 4 mm lateral to the midline, at a depth of 1.5 to 1.7 mm from the cortical surface) to anterogradely label the CST which sprouts axons and crosses the midline into the denervated spinal cord after TBI and EPO treatment. D–G: Representative pictures from the cervical spinal cord showing midline-crossing BDA-labeled CST axons (arrow in E) sprouting into denervated side of the ventral gray matter in a rat after TBI. EPO treatment significantly increases the axon crossing (arrow in G). H–K: Representative pictures from the lumbar spinal cord showing midline-crossing BDA-labeled CST axons (arrow in I) sprouting into denervated side of the ventral gray matter in a rat after TBI. EPO treatment significantly increases the axon crossing (arrow in K). L: Quantitative data showing that no obvious BDA-labeled axons were observed in the opposite site of the cervical and lumbar spinal cord in sham rats, whereas the number of contralesional CST in the denervated cervical and lumbar gray matter were significantly increased by traumatic injury (P < 0.05 vs. Sham) and EPO treatment (P < 0.05 vs. Saline). CC: central canal. Scale bar = 2 mm in A, 200 μm in B, 100 μm in D (applicable to E, F, H, I, and J) and 50 μm in G (applicable to K). Data represent mean ± SD. N = 8 (Sham); 8 (Saline); 8 (EPO).