Figure 2From: Muscle atrophy induced by SOD1G93A expression does not involve the activation of caspase in the absence of denervationMuscle atrophy is exacerbated in denervated mice. (A) Immunofluorescence analysis of myosin heavy chain (MyHC)-slow (green) and laminin (red) performed on soleus muscles of WT, MLC/SOD1G93A, WT-denervated and SOD1G93A muscle at age 123 days, which corresponded to the paralysis stage in SOD1G93A mice. Bar, 50 μm. (B) Real-time polymerase chain reaction (PCR) for nicotinic acetylcholine receptor (AChR)-γ expression in both WT and MLC/SOD1G93A transgenic muscle. **P = 0.006. (C) Representative Western blot analysis (left) for glial fibrillary acidic protein (GFAP) expression in the spinal cord of WT, MLC/SOD1G93A and SOD1G93A transgenic mice at 123 days old. Immunoblotting for β-actin served as a control for protein loading. Right: Densitometric analysis of seven separate immunoblot experiments showing the expression levels of GFAP calculated as ratios of GFAP/β-actin expression. **P < 0.005.Back to article page