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. 2015 Mar 12;34(9):1231–1243. doi: 10.15252/embj.201490578

Figure 2. FGF22 deficiency impairs bouton formation and circuit remodeling after spinal cord injury.

Figure 2

  1. Schematic representation of CST detour circuit formation following a mid-thoracic dorsal bilateral hemisection of the spinal cord.
  2. Confocal images of hindlimb CST collaterals exiting the main CST tract (arrows) in the cervical spinal cord 3 weeks following a T8 dorsal bilateral hemisection in FGF22-competent (left panel) and FGF22-deficient (right panel) mice. Scale bar equals 40 μm.
  3. Quantification of the number of exiting hindlimb CST collaterals per labeled hindlimb CST fiber at 3 weeks following T8 dorsal bilateral hemisection in FGF22-competent and FGF22-deficient mice (n = 8 animals per group). Mean ± SEM. No significant differences between the groups were detected (unpaired two-tailed t-test).
  4. Confocal images showing putative synaptic boutons (arrows) on newly formed cervical hindlimb CST collaterals at 3 weeks following spinal cord injury in FGF22-competent (left panel) and FGF22-deficient (right panel) mice. Scale bar equals 20 μm.
  5. Quantification of bouton density on newly formed cervical hindlimb CST collaterals in FGF22-competent and FGF22-deficient mice (n = 8 animals per group) at 3 weeks after injury. Mean ± SEM. *P = 0.0244 (unpaired two-tailed t-test).
  6. 3D Rendering of a confocal image stack that illustrates putative synaptic contacts between CST collaterals (green) and LPSN (red) counterstained with NeuroTrace 435/455 (blue). Scale bar equals 30 μm.
  7. Quantification of the percentage of LPSN contacted by cervical hindlimb CST collaterals in FGF22-competent and FGF22-deficient mice at 3 weeks after injury (n = 8 animals per group). Mean ± SEM. ***P = 0.0001 (unpaired two-tailed t-test).