Figure 1.

Transient upregulation of p-STAT3 expression in cortical neurons does not contribute to endogenous CST remodelling after injury. (A–D) Confocal images of the expression of the activated form of STAT3, p-STAT3, in layer V cortical neurons (green, NeuroTrace 435; red, p-STAT3) of unlesioned (A), lesioned STAT3-competent (B, 24 h after lesion; C, 3 w after lesion) and STAT3-deficient mice (D). Arrows indicate p-STAT3-positive neurons (magnified in insets). (E) Quantification of p-STAT3 expression in layer V cortical neurons of unlesioned mice (white bar, n=5) and mice perfused at different timepoints following thoracic hemisection (grey bars, STAT3-competent mice; blue bar, STAT3-deficient mice; n=5–6 for each timepoint). (F) Schematic representation of the analysis of CST remodelling after a mid thoracic hemisection. (G,H) Quantification of axonal sprouting in the cervical spinal cord (G) and of the percentage of long propriospinal neurons contacted by CST fibres (H) in STAT3-competent (grey bars, n=9) and STAT3-deficient (blue bars, n=12) mice perfused 3  w following thoracic hemisection. All bars and error bars in this figure represent mean±s.e.m. Statistical analysis was performed using a one-way ANOVA with Tukey test for E (left panel) and t-tests for E (right panel), G, H. *P<0.05. Scale bars equal 50 μm in B (also for A) and in D (also for C). ANOVA, analysis of variance; CST, corticospinal tract; SC, spinal cord; STAT3, signal transducer and activator of transcription 3.