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Figure 8 | BMC Genomics

Figure 8

From: The human G93A-SOD1 mutation in a pre-symptomatic rat model of amyotrophic lateral sclerosis increases the vulnerability to a mild spinal cord compression

Figure 8

Expression of neurofilament heavy chain and synaptophysin in ventral spinal cord at 24 hours after compression SCI. Neurofilament heavy chain (Nfh; clone N52) staining of spinal cord sections is clearly visible in motor neurons (arrows) and adjacent axons in both WT (A) and G93A-SOD1 (B) which is significantly stronger in the G93A-SOD1 (* P = 0.03; E). Scale bar = 100 μm. Transverse sections are taken within a segment 10 mm caudal to the injury epicenter. Synaptophysin (SYN) immunoreactive synaptic boutons (arrows) can be seen surrounding unstained motor neuron cell bodies in both WT (C) and G93A-SOD1 (D) spinal cord, with no difference in SYN distribution between the two genetic types. The intensity of staining is non-significantly different between the G93A-SOD1 and wild type spinal cords (F). Scale bar = 25 μm. SCI-SOD1: spinal cord tissue from rats over-expressing the G93A-SOD1 gene mutation. SCI-WT: spinal cord tissue from WT rats. Western blot of spinal cord rostral to the injury epicenter obtained from WT and G93A-SOD1 rats. Three spinal cord samples for both WT and G93A-SOD1 were used (G). A significant increase in Nfh (clone 52) expression levels can be detected in G93A-SOD1 rats compared to WT rats with β-actin as the internal control (* P = 0.041; H).

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