(A) HeCS significantly increased NGF in muscularis externa and mucosa/submucosa, which was blocked by inhibition of α1/α2 and β1/β2-adrenergic receptors prior to each daily stress session. n=8 rats in each group, *p<0.01, control (Ctr) vs. HeCS and HeCS vs. HeCS + adrenergic receptor antagonists. (B) Immunohistochemical staining for NGF (brown) in distal colon cross-sections from control and HeCS rats. Sections were counterstained with hematoxilyn. (C) NGF antagonism by systemic administration of neutralizing antibody significantly reduced HeCS-induced increase in visceromoter response. HeCS, n=4 rats, HeCS + NGF Ab, n=5 rats, *p<0.05 baseline vs HeCS; +p<0.05 HeCS vs. HeCS + NGF Ab. (D) Intrathecal administration of trkA antagonist k252A (n=5) or antisense oligonucleotide (n=3) suppressed HeCS-induced increase in visceromoter response. *p<0.05 baseline vs. HeCS, +p<0.05, HeCS + mismatch oligonucleotide (MM) vs. HeCS + NGF Ab. (E) Western blots showing the effects of intrathecal treatment with either trkA antisense (AS) or mismatch (MM) oligonucleotide on trkA receptor expression in thoracolumbar (TL), thoracic (Th) or lumbosacral (LS) DRG. n=4, *p<0.05 mismatch vs antisense oligonucleotides.