Figure 9.

Working model for the contribution of CSPGs effects on growth cone mitochondria to the suppression of axon elongation. Under control conditions growth cones contain a normal content of normally respiring mitochondria resulting in sufficient ATP production to maintain steady axon elongation. CSPGs result in a decrease in the number of mitochondria targeting to growth cones and a suppression of their respiration. Inhibition of the interaction between dynein and dynactin (using CC1) increases the number of mitochondria at growth cones, but is not expected to affect their respiration, and results in partial increases in axons lengths on CSPGs (see bottom graph). When mitochondria respiration is promoted (ALC treatment) in conjunction with CC1 expression the effects of CSPGs on axon elongation further suppressed. The arrows in the graph below CC1 and CC1+ALC denote the detected increases in axon lengths relative to CSPGs. However, as CSPGs are expected to continue inhibiting pathways that promote elongation, and drive the activity of pathways that inhibit elongation, the restoration of mitochondrial parameters only has partial effects on axon elongation, as shown by the bottom graph depicting the overall effects of treatments on axon lengths.