Figure 3
Dorsal column lesion triggers the formation of relays circuits between DRG exiting collaterals and relay neurons originating from the cuneate nucleus. (a) Experimental setup of the analysis of the formation of relay circuits. (b) Confocal image of cuneate nucleus projecting neurons in the cervical spinal cord following dorsal column lesion and quantification of the percentage of cuneate nucleus projecting neurons contacted by DRG collaterals in unlesioned (control) of lesioned mice at 21 and 84dpi (left panel). Quantification of the localization of cuneate nucleus projecting neurons in unlesioned (control) of lesioned mice at 21 and 84dpi (right panel). (c) Representative confocal images of appositions between cuneate nucleus projecting neurons and DRG collaterals in the cervical spinal cord (arrows point to appositions). Quantifications of the % of contacted cuneate nucleus projecting neurons (left) in unlesioned (control) of lesioned mice at 21 and 84dpi (left panel, p = 0.0378) and quantifications of the localization of contacted cuneate nucleus projecting neurons (%, right p = 0.0408 dorsal laminae control vs 12 weeks). (d) Representative confocal images of appositions between relay neurons and DRG collaterals and quantifications (left) of the number of contacts per cuneate nucleus projecting neuron (p = 0.0041 control vs 3 weeks and p = 0.00002 control vs 12 weeks). Quantification of the total number of contacts per time points (**: p < 0.01 control vs 3 weeks and *p < 0.05 control vs 12 weeks). Data distribute normally and were analyzed using 1-way ANOVA followed by Dunnett’s multiple comparisons test. Scale bars equal 300 µm in (b), 50 µm in ((c); right panel is a 3-times magnification of the boxed area) and 15 µm in (d).
