Colonic
inflammation has profound effects on the urinary bladder physiology and produces
hypersensitivity of bladder afferent neurons and
neurogenic bladder overactivity.
Calcitonin gene-related peptide (CGRP) expressed in dorsal root ganglia (DRG) plays an important role in mediating sensory perception following visceral
inflammation. In the present study, we determined that the expression of CGRP was increased in bladder afferent neurons in lumbosacral DRG following tri-
nitrobenzene sulfonic acid (TNBS)-induced
colitis in rat. After
colitis, the percentage of bladder afferent neurons expressing CGRP was increased in L1 (61.2+/-2.9% in
colitis vs. 37.7+/-5.1% in controls; p<0.05) and S1 DRG (26.3+/-2.3% in
colitis vs. 15.5+/-1.9% in controls; p<0.01). We also demonstrated that the expression of
tyrosine kinase receptor TrkB was increased in L1 (39.7+/-2.9% in
colitis vs. 25.2+/-4.3% in controls; p<0.05) and S1 DRG (45.6+/-3.8% in
colitis vs. 38.3+/-3.6% in controls; p<0.01) following
colitis. CGRP and TrkB were co-stored in a subpopulation of DRG neurons in control and colitic animals and the number of DRG cells co-expressing CGRP and TrkB was significantly increased in L1 (2.7-fold, p<0.01) and S1 DRG (2.4-fold, p<0.01) following
colitis. In cultured DRG, exogenous
BDNF application significantly increased CGRP expression, which was blocked by TrkB selective inhibitor
K252a. These results suggest that up-regulation of CGRP and TrkB in bladder afferent neurons may play a role in colon-to-bladder cross-sensitization following
colitis.