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. Author manuscript; available in PMC: 2017 Nov 1.
Published in final edited form as: Exp Neurol. 2015 Dec 11;285(Pt B):126–135. doi: 10.1016/j.expneurol.2015.12.006

Figure 2. CREB activity was increased in bladder afferent neurons and was regulated by endogenous BDNF post colitis.

Figure 2

Immunostaining of DRG segments containing bladder afferent neurons (A and D, blue cells) showed that CREB phosphoryaltion (B and E, red nuclear stain) was expressed in bladder afferent neurons (C and F, purple cells indicated by arrows) in both control animals (A–C) and animals treated with TNBS (D–F). CREB phosphorylation was increased in bladder afferent neurons at 7 days and 21 days post colitis induction (G, animal numbers: control: 5, TNBS 7 days, 4; TNBS 21 days, 4), which was reduced in BDNF+/− rats (G, open bar, n=4). The level of CREB phosphorylation in the DRG (L1–L2 and L6–S1) was also compared between wildtype and BDNF+/− rats by western blot (H, n=3) showing attenuation of CREB phosphorylation by BDNF partial deletion in vivo. *, p<0.05 vs. control; #, p<0.05 vs TNBS 21 days. Calibration bar = 80 μm.