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Fig. 4 | BMC Neuroscience

Fig. 4

From: Shift in the function of netrin-1 from axon outgrowth to axon branching in developing cerebral cortical neurons

Fig. 4

Quantitative morphometric analysis of outgrowth, branching, and filopodial protrusion in E14 and E16 cortical axons (A, B). Netrin-1-induced outgrowth of E14 axons and branching of E16 axons. The numbers of branch points (with branches longer than 12 μm and/or lamellipodium-tipped) were counted along the whole length of each primary axon. Error bars indicate the SEM (n = 25 from 3 experiments in E14 neurons, and from 4 experiments in E16 neurons). a, b and c: significantly higher than a′, b′ and c′, respectively, by Steel–Dwass test which was employed for comparisons among 3 test groups, within either E14 or E16 axons (p < 0.05). Besides, the length of primary axon (A) as well as the numbers and density of branch points (B) were compared between E14 and E16 axons: *p < 0.05 and **p < 0.01 by Wilcoxon rank sum test, which was employed for comparisons between E14 and E16 axons subjected to the same treatment out of the three (that is, under basal conditions or after 4 h netrin-1 stimulation in the absence or presence of an anti-DCC antibody). C Abundance of protrusions on the shafts of mouse E14 cortical axons under basal conditions. The numbers of filopodial protrusions (12 μm or shorter and lacking a lamellipodial tip) were counted along the whole length of each primary axon. Data were obtained from the sets of axons under basal conditions analyzed in A and B (25 per test group), and the numbers and densities of protrusions were compared between E14 and E16 axons. Error bars indicate the SEM. *p < 0.05 by Wilcoxon rank sum test

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