Figure 11.

Cell death in denervated neurons in the CA1 region is induced by similar mechanism as in the axotomized neurons. a–d, Ratio of cleaved caspase-3-positive neuronal number to total neuronal number obtained by blind stereological counting in the CA1 region, percentage of unlesioned control ratio value. a, TrkB-Fc induces a significant increase in apoptotic neuronal number in the lesioned, but not unlesioned, slices at 1 d after the injury; n = 43 slices/4800 neurons; **p = 0.013, one-way ANOVA and Bonferroni's post hoc analyses. b, Treatment with function-blocking antibodies to p75^NTR (Fig. 2b) abolished the increase in the number of apoptotic neurons promoted by TrkB-Fc; n = 46 slices/4890 neurons; **p = 0.002, one-way ANOVA and Bonferroni's post hoc analyses. c, Treatment with plasmin abolished the TrkB-Fc-induced increase in the number of apoptotic neurons; n = 33 slices/3990 neurons; **p = 0.004, one-way ANOVA and Bonferroni's post hoc analyses. d, Bumetanide abolishes the death induction in neurons deprived of BDNF; n = 33 slices/3750 neurons; **p = 0.007, one-way ANOVA and Bonferroni's post hoc analyses. e, f, Ratio of p75^NTR-positive neuronal number to total neuronal number, obtained by blind stereological counting in the CA1 region, percentage of unlesioned control ratio value. e, The amount of p75^NTR-positive neurons was increased after axotomy only in the presence of TrkB-Fc; the increase was fully blocked by bumetanide; n = 56 slices/7800 neurons; **p = 0.032, one-way ANOVA and Bonferroni's post hoc analyses. f, ROCK inhibitor Y-27632 completely abolished posttraumatic p75^NTR upregulation in the presence of TrkB-Fc; n = 58 slices/5840 neurons; **p = 0.002 (lesioned plus TrkB-Fc), one-way ANOVA and Bonferroni's post hoc analyses. Error bars indicate SEM.