Figure 11.

Depletion of tau from hippocampal neurons increases the numbers of axonal branches by a mechanism that does not require spastin. Neurons were treated with either control siRNA, tau siRNA, spastin siRNA, or a combination of tau siRNA and spastin siRNA. (A) Pie graphs showing the ratio of hippocampal neurons in stage 1, stage 2, or stage 3 in each experimental group (n > 200). More neurons remained in stage 1 or stage 2 in spastin-depleted cultures than in control cultures. There is no significant difference between the tau-depleted group and the control group or between the spastin+tau-double-depleted group and the control group. (B) Quantitative analyses of the number of minor processes in stage 3 hippocampal neurons. Only in the tau siRNA treated group does the number increase by 28% (p < 0.001). Compared with control, the other two groups showed no significant difference (p > 0.05; n > 200). (C) Quantitative analyses of axonal lengths of stage 3 hippocampal neurons. Compared with control, axonal lengths decrease by 11% (p < 0.01), 12% (p < 0.01), and 16% (p < 0.01) in the spastin-depleted group, the tau-depleted group, and the spastin+tau-double depleted group, respectively (n > 200). (D) Quantitative analyses of number of primary axonal branches in stage 3 hippocampal neurons. For quantification of branches, we chose stage 3 neurons with axons 100–150 μm in length. Compared with the control group, there is a 40% (p < 0.01) decrease in the number of axonal branches in the spastin-depleted group and a 56% (p < 0.0001) increase of the number of axonal branches in the tau-depleted group. There is no significant difference between the control and spastin+tau-double-depleted groups (p > 0.05; n > 200).