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. 2010 Oct;27(10):1793–1803. doi: 10.1089/neu.2010.1351

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Copyright 2010, Mary Ann Liebert, Inc.

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FIG. 4. — (A) Neurofilament (NF)-H and NF-L mRNA were assessed in spinal cord injury (SCI) rats with and without spontaneous pain (n = 4 per group) using DNA microarrays (a method previously described in Nesic et al., 2005). mRNA levels of NF-H and NF-L were significantly increased (*p < 0.05) in five segments rostral from the site of injury. mRNA values were normalized to the levels of mRNAs in SCI rats without pain (set to = 1; mean ± standard deviation). Similarly significant increases in NF mRNAs were also found in five segments caudal from the site of injury (data not shown). (B) A representative example of SMI-31 labeling in sham rats (B_I), vehicle-treated SCI rats (B_II), and VEGF₁₆₅-treated SCI rats (B_III), that were classified as SCI rats that developed pain (scale bar = 500 μm; T6 segment at 8 weeks post-injury). Normal labeling for SMI-31 (Sham) was significantly lower in vehicle-treated and VEGF₁₆₅-treated SCI rats. However, VEGF₁₆₅-treated SCI rats had visibly more SMI-31-labeled axons in the dorsal columns (marked with arrows), and dorsal horns, than vehicle-treated SCI rats. (B_IV–B_VI) SMI-31-labeled thick myelinated axons are widely scattered in sham and vehicle-treated dorsal horns, but are visibly increased in the dorsal horns of VEGF₁₆₅-treated cords (scale bar = 200 μm). (C) Quantitative analysis of SMI-31 labeling in the dorsal columns of spinal cord segments around the site of injury (T6–T10) in three experimental groups (n = 6 animals per group). Sham animals had significantly more SMI-31 labeling compared to both vehicle-treated and VEGF₁₆₅-treated animals (average ± standard deviation; **p < 0.0001; values normalized to sham = 1). However, VEGF₁₆₅-treated SCI rats had significantly more SMI-31-labeled axons in the dorsal columns than vehicle-treated SCI rats (*p < 0.01). (D) Semi-quantitative analysis of SMI-31 labeling in the dorsal horns in the same sections used for the analysis shown in C. (average ± standard deviation; *p < 0.05; values normalized to sham = 1). SCI pain was associated with significant twofold increases in SM-31 labeling (p < 0.05) in the dorsal horns, while VEGF₁₆₅-induced SCI pain was associated with additional significant increases in SM-31 labeling (2.5-fold; p < 0.05; VEGF, vascular endothelial growth factor).

FIG. 4. — (A) Neurofilament (NF)-H and NF-L mRNA were assessed in spinal cord injury (SCI) rats with and without spontaneous pain (n = 4 per group) using DNA microarrays (a method previously described in Nesic et al., 2005). mRNA levels of NF-H and NF-L were significantly increased (*p < 0.05) in five segments rostral from the site of injury. mRNA values were normalized to the levels of mRNAs in SCI rats without pain (set to = 1; mean ± standard deviation). Similarly significant increases in NF mRNAs were also found in five segments caudal from the site of injury (data not shown). (B) A representative example of SMI-31 labeling in sham rats (B_I), vehicle-treated SCI rats (B_II), and VEGF₁₆₅-treated SCI rats (B_III), that were classified as SCI rats that developed pain (scale bar = 500 μm; T6 segment at 8 weeks post-injury). Normal labeling for SMI-31 (Sham) was significantly lower in vehicle-treated and VEGF₁₆₅-treated SCI rats. However, VEGF₁₆₅-treated SCI rats had visibly more SMI-31-labeled axons in the dorsal columns (marked with arrows), and dorsal horns, than vehicle-treated SCI rats. (B_IV–B_VI) SMI-31-labeled thick myelinated axons are widely scattered in sham and vehicle-treated dorsal horns, but are visibly increased in the dorsal horns of VEGF₁₆₅-treated cords (scale bar = 200 μm). (C) Quantitative analysis of SMI-31 labeling in the dorsal columns of spinal cord segments around the site of injury (T6–T10) in three experimental groups (n = 6 animals per group). Sham animals had significantly more SMI-31 labeling compared to both vehicle-treated and VEGF₁₆₅-treated animals (average ± standard deviation; **p < 0.0001; values normalized to sham = 1). However, VEGF₁₆₅-treated SCI rats had significantly more SMI-31-labeled axons in the dorsal columns than vehicle-treated SCI rats (*p < 0.01). (D) Semi-quantitative analysis of SMI-31 labeling in the dorsal horns in the same sections used for the analysis shown in C. (average ± standard deviation; *p < 0.05; values normalized to sham = 1). SCI pain was associated with significant twofold increases in SM-31 labeling (p < 0.05) in the dorsal horns, while VEGF₁₆₅-induced SCI pain was associated with additional significant increases in SM-31 labeling (2.5-fold; p < 0.05; VEGF, vascular endothelial growth factor).