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. 2011 Aug 4;20(21):4116–4131. doi: 10.1093/hmg/ddr335

Figure 2.

Figure 2.

Elimination of TrkB in motor neurons increases lifespan, slows disease progression, delays the onset of paralysis and improves locomotor function in G85R SOD1 mice. (A) Cre-mediated deletion of TrkB in adult motor neurons increases lifespan of male G85R-SOD1+/−; VAChT-Cre+/− mice (384 ± 7 days) compared with G85R-SOD1+/−; VAChT-Cre−/− mice (358 ± 8 days) (P < 0.05). (B) Deletion of TrkB in motor neurons increases lifespan of female G85R-SOD1+/−; VAChT-Cre+/− mice (363 ± 7 days) compared with G85R-SOD1+/−; VAChT-Cre−/− mice (335 ± 9 days) (P < 0.05). (C and D) Conditional deletion of TrkB in motor neurons did not influence age of disease onset of G85R mutant SOD1 mice. (E and F) Progression through (D) and duration (E) of an early disease phase was slower and longer in G85R-SOD1+/−; VAChT-Cre+/− mice. (G) The onset of paralysis was delayed in G85R-SOD1+/−; VAChT-Cre+/− mice (361 ± 7 days) compared with G85R-SOD1+/−; VAChT-Cre−/− mice (340 ± 6 days) (P < 0.05). (H) At the peak of bodyweight, G85R-SOD1+/−;VAChT-Cre+/− mice stayed significantly longer on rotarod beam (272 ± 19 s) than G85R-SOD1+/−; VAChT-Cre−/− mice (197 ± 27 s) (P < 0.05). (I) At the age of 2 weeks after the peak of bodyweight, G85R-SOD1+/−; VAChT-Cre+/− mice continued to stay significantly longer on rotarod beam (246 ± 25 s) than G85R-SOD1+/−; VAChT-Cre−/− mice (179 ± 24 s) (P < 0.05).