Figure 3
From: Lack of a synergistic effect of a non-viral ALS gene therapy based on BDNF and a TTC fusion molecule
Transport efficiency of BDNF-TTC molecule. A. Immunohistochemical labeling for BDNF expression in the grey matter of the ventral horn of of (a) positive control (SOD1G93A transgenic mice injected with empty plasmid), (b) SOD1G93A-BDNF and (c) L2 and (d) L4 spinal segments of SOD1G93A-BDNF-TTC mice. Note that BDNF is only expressed in the L2 spinal cord sections of mice treated with BDNF-TTC chimera and does not appear in other spinal cord segments. (e, f) Detail of BDNF immunolabeling of the sections shown in c and d, at higher magnification. Presence of TTC in the grey matter of the ventral horn of (g) SOD1G93A-BDNF-TTC and (h) SOD1G93A-TTC treated mice. Note more intense TTC labeling in animals treated with the chimera. Arrows point to some of the neurons positively stained for TTC. Bar = 200 μm in a, b, c, d, g and h; bar = 100 μm in e and f. B. Real-time PCR assay of a synaptic transmission-related gene in spinal cord specimens of symptomatic SOD1G93A mice. Fold-changes in the expression of GABA(A) receptor subunit-4 (Gabra4) mRNA levels in total spinal cord of wild-type (negative control), positive control and treated transgenic mice. Results showed a significant down-regulation of the expression of this gene in neurotrophin-bearing treatments (BDNF-TTC and BDNF), approaching wild-type levels (*P < 0.05, **P < 0.01; error bars indicate SEM).