Transgenic expression of Nfil3 in neurons in SOD1G93A mice attenuates degeneration of motor axons.
a, L5 ventral root sections derived from 180- to 190-day-old SOD1G93A mice overexpressing Nfil3 (Nfil3/SOD1G93A-tg), SOD1G93A mice (SOD1G93A-tg), and wild-type mice were stained with antibodies against Tuj1 (red/white) and myelin basic protein (MBP, green). Representative images are shown. Images of L5 ventral root sections derived from SOD1G93A mice at the end stage are also shown. The bottom panels are magnified views. Scale bars = 200 μm. b, the number of motor axons was counted and is presented as mean ± S.E. n = 3 (one male and two females) for wild-type, 4 (four males) for SOD1G93A-tg, 3 (three males) for Nfil3/SOD1G93A-tg, and 3 (one male and two females) for SOD1G93A-tg at the end stage. *, p < 0.05 by two-tailed t test. c, lumbar spinal cord sections derived from SOD1G93A-tg, Nfil3/SOD1G93A-tg, and wild-type mice at 220–230 days of age were immunostained with Neurofilament H (SMI32) and GFAP antibodies. d, the number of large motor neurons per section was counted and is presented as mean ± S.E. Data were obtained from three mice (two males and one female). *, p < 0.05; ***, p < 0.001 by two-tailed t test. Mean GFAP fluorescent intensity in the ventral horn per section was quantified and is presented as mean ± S.E. Data were obtained from three mice (two males and one female). *, p < 0.05; **, p < 0.01 by two-tailed t test.