Muscle 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.