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

Figure 4. Deletion of forebrain FGFR1 and FGFR2 expression impairs bouton formation and circuit remodeling after spinal cord injury.

Figure 4

  1. Confocal images of hindlimb CST collaterals exiting the main CST tract (arrows) in the cervical spinal cord 3 weeks following T8 dorsal bilateral hemisection in FGFR-competent (left panel), forebrain FGFR1-deficient (middle panel), and forebrain FGFR2-deficient (right panel) mice. Scale bar equals 40 μm.
  2. Confocal images of hindlimb CST collaterals exiting the main CST tract (arrows) in the cervical spinal cord 3 weeks following T8 dorsal bilateral hemisection in FGFR-competent (left panel) and hindlimb motor cortex FGFR1/FGFR2 double-deficient (right panel) mice. Scale bar equals 40 μm.
  3. Quantification of the number of exiting hindlimb CST collaterals at 3 weeks following T8 dorsal bilateral hemisection in forebrain FGFR single-deficient mice, hindlimb motor cortex FGFR1/FGFR2 double-deficient mice, and the corresponding FGFR-competent control mice (n = 6–15 animals per group). Mean ± SEM. *P < 0.05; ***P < 0.001 (ANOVA followed by Tukey tests for FGFR-competent versus FGFR single-deficient mice). No significant differences were found between FGFR-competent and FGFR1/FGFR2 double-deficient mice (unpaired two-tailed t-tests).
  4. Confocal images showing putative synaptic boutons (arrows) on newly formed cervical hindlimb CST collaterals at 3 weeks following spinal cord injury in FGFR-competent (left panel), forebrain FGFR1-deficient (second panel from left), forebrain FGFR2-deficient (second panel from right), and hindlimb motor cortex FGFR1/FGFR2 double-deficient (right panel) mice. Scale bar equals 20 μm.
  5. Quantification of the bouton density on newly formed cervical hindlimb CST collaterals in FGFR-competent, forebrain single FGFR-deficient, and hindlimb motor cortex FGFR1/FGFR2 double-deficient mice (n = 6–16 animals per group). Mean ± SEM. *P < 0.05, **P < 0.01 (ANOVA followed by Tukey tests in case of multiple group comparisons, e.g. FGFR-competent versus FGFR single-deficient mice). **P = 0.0028 (unpaired two-tailed t-tests for comparisons of FGFR-competent versus FGFR1/FGFR2 double-deficient mice).
  6. Quantification of the percentage of LPSN contacted by hindlimb CST collaterals in FGFR-competent, forebrain single FGFR-deficient, and hindlimb motor cortex FGFR1/FGFR2 double-deficient mice (n = 6–16 animals per group). ***P < 0.0001 (unpaired two-tailed t-tests for comparisons of controls versus FGFR1/FGFR2 double-deficient mice). No significant differences were found between FGFR-competent and FGFR single-deficient mice (ANOVA followed by Tukey tests).