Fig. 6
From: In vivo imaging of injured cortical axons reveals a rapid onset form of Wallerian degeneration
A local NAD+-dependent pathway controls cortical axon WD. a, b Representative examples of a lesioned WldS–Thy1-L15 and WT axons of comparable distal length. c WldS axons have a significantly later fragmentation onset time than WT axons, WldS, n = 24 axons, 11 mice; WT n = 21 axons, 13 mice, ** p < 0.01. d The fragmentation rates are not significantly different in WT and WldS axons although the data suggested a trend towards faster fragmentation in the WldS axons. e Representative images of a lesioned axon in cortical slice culture treated with NAD+. f Fragmentation onset time in lesioned axons in cortical slice cultures is significantly earlier in axons < 600 μm (roWD, blue, n = 9 axons, 5 slices, 5 mice) than axons > 600 μm in length (WD, grey, n = 8 axons, 6 slices, 2 mice), *** p < 0.001. g–i Degeneration of in vitro lesioned axons with no treatment (control, g), with addition of NAD+ prelesion (h) and postlesion (i). Blue dotted line shows the 24 h time point. j Axons are protected by NAD+ when added both before or after the lesion. Mean ± SEM. Mann Whitney U test. Scale bar 70 μm (a, b), 100 μm (e)