Fig. 5

Fig. 5 Hdac1 function is necessary for regenerative neurogenesis downstream of immune system activity Cross sections for (A and B) at 24 hpl; lateral views for (C, D, and F) at 48 hpl are shown; asterisks indicate the injury site; arrows indicate double-labeled cells; boxed areas are shown in higher magnification on the right. All incubations were from 0 to 48 hpl. (A and B) The fluorescent in situ hybridization (ISH) signal for hdac1 is stronger in the spinal cord proximal to the injury site than distal to it (arrows in A). Proximal to the injury site, the hdac1 ISH signal overlaps with GFP immunohistochemistry (IHC), detecting the her4.3:GFP transgene. (C) TSA and mocetinostat reduce the number of newly generated motor neuron progenitor ERGs (olig2:GFP+/EdU+); example images and quantification are shown (one-way ANOVA; p < 0.0001; Tukey’s post-test: ∗∗∗p = 0.0005; ∗∗∗∗p < 0.0001). (D and E) TSA reduces the number of newly generated motor neurons (mnx1:GFP+/EdU+) after spinal injury; example images in (D), quantification in (E) (t test ∗∗∗∗p < 0.0001). (F) Mocetinostat treatment reduces the number of newly generated motor neurons after injury (Mann-Whitney U test ∗∗∗p = 0.0002). (G) Mocetinostat co-application partially suppresses LPS-induced increase in motor neuron generation after injury (one-way ANOVA p < 0.0001; Holm-Sidak’s post-test ∗∗∗∗p < 0.0001; ∗p = 0.0463; ns, p = 0.0643). Scale bars: (A and B): 50 μm, inset 25 μm; (C, D, and F): 50 μm, insets: 10 μm. Data are represented as mean ± SEM (see also Figure S4).