Figure 5. (A-E) Vehicle-treated model rats exhibited pronounced reactive gliosis as revealed by TRITC-conjugated GFAP immunofluorescence staining. SP: spinal cord. (A) Normal astrocytes in the spinal cord. (B) Glial scarring following L-BMAA injection in the vehicle-treated model group. (C-E) C16+Ang-1treatment alleviated reactive astrogliosis. (Q) L-serine treatment resulted in fewer abnormally proliferating astrocytes, and the combined treatment produced more pronounced effects according to cell quantification. (F, K, P) In normal control rats, intense GLT-1 labeling appeared in astrocytes around neurons of the DG region of the hippocampus and ventral horn motor neurons (arrow in P), in contrast to the pronounced decrease in GLT-1 labeling around ventral horn motor neurons in the vehicle-treated model rats. Treatment with C16+Ang-1, L-serine, and especially combined treatment with both results significantly increased expression of GLT-1. Scale bar = 100 μm. (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.