Figure 6.

Adult spinal cord neurogenesis and nociception show similar BDNF dependence. (A) Immunofluorescence analysis of adult rat spinal cord, showing that BDNF treatment suppresses the expression of neurogenic markers Mash1, DCX and Notch3, week 6 post-CCI (compare with Fig. 1C, week 6). Quantification shown as mean ± SEM, n = 5 rats per treatment. Statistically significant differences shown for BDNF versus Veh, for ipsilateral and contralateral sides respectively (two-tailed t-test); scale bars: 200 μm. (B) BDNF treatment increases nociceptive threshold in both CCI and Sham rats. (C) BDNF administration extends CCI-induced hyperalgesia, preventing the typical recovery 2 months after CCI. (D) A delay in BDNF administration for 3 weeks post-CCI produces initially a brief decrease in nociceptive threshold, followed by a long-term increase. (E) A 3-week delay in BDNF administration increases long-term withdrawal latency in CCI rats, relative to administration beginning at day 0 (compare to C). BDNF-induced hyperalgesia in Sham rats remains similar to day 0 administration. Allodynia and hyperalgesia were measured daily during first week of BDNF administration, and weekly thereafter.