Figure 9. After the rats had received injections of 300 mg/kg BMAA each day for 3 days, morphological changes were observed in the motor neurons of the lumbar ventral horn (A-O), hippocampus (P-T), and brain motor cortex (U-Y) at 2w, 4w and 8w post-injection. NF-200 (red, a specific marker for neurofilament in neurons) and MBP (green, a specific marker for myelin) double immunolabeling, which recognizes neurofilament proteins pivotal for maintaining large neurons with extensively myelinated processes, allowed visualization of changes in somatic and dendritic morphology and revealed structural injury. Scale bar = 100 μm. In the vehicle-treated model group, extensive disintegration of dendritic processes and a lack of NF-200 staining both in somatic and dendrites of neurons as well as atrophy of lumbar ventral horn motor neurons were noted (L); a drastic decrease in NF-200 staining was also discernible at 2 months after L-BMAA injection in the hippocampus (Q) and motor cortex (V). However, C16+Ang-1 and L-serine treatments could attenuate the loss of axons in the CNS after L-BMAA administration, and the combined treatment produced the most pronounced effects. Transverse sections of the anterior horn of the lumbar spine are denoted with SP, and coronal sections of the motor cortex are denoted with BC. (I-III) Quantification of relative fluorescence of NF200-positive cells. (a) p<0.05 vs normal rats; (b) p<0.05 vs vehicle-treated rats; (c) p<0.05 vs. C16+Ang-1–treated rats; (d) p<0.05 vs. L-serine–treated rats.