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. 2002 Jun 15;22(12):4825–4832. doi: 10.1523/JNEUROSCI.22-12-04825.2002

Fig. 4.

Fig. 4.

Compared with single-transgenic hMg-SOD1(G93A) mice, double-transgenic hMg-SOD1(G93A)/Thy1-SOD1(G93A) mice express at least twice the amount of mutant SOD1(G93A) in postnatal neurons but exhibit no acceleration of motoneuron pathology or disease. The immunoblot analysis of human (h) and mouse (m) SOD1 in spinal cord (S.CORD) from 1 month Thy1-SOD1(G93A) line 13, hMg-SOD1(G93A), and double-transgenic hMg-SOD1(G93A)/Thy1-SOD1(G93A) mice was as described in Figure 1C. Force was determined as described for Figure 1J, and the values are averages from two mice each. Lumbar spinal cord ubiquitin deposits and areas of GFAP-immunoreactive cells were analyzed as described in Materials and Methods. Values are averages from 40 (ubiquitin) and 50 (GFAP) spinal cord sections; data from two mice each were pooled. The quantitative analysis of muscle denervation (p75: mLGC) was as described for Figure2D,E. All transgenic mice analyzed in the figure expressed the SOD1(G93A) mutant protein.