POST INFLAMMATORY VISCERAL HYPERSENSITIVITY DEPENDS ON NERVE GROWTH FACTORS AND THE SENSORY NEUROPEPTIDE CGRP

Visceral hypersensitivity is a common feature of functional diseases, with a variable central and/or peripheral component. Colitis induced by the installation of trinitrobenzene sulfonic acid (TNBS) is a frequently used model of peripherally driven hypersensitivity. Antibodies to nerve growth factor are known to inhibit post inflammatory hypersensitivity in both visceral and somatic territories. Calcitonin gene related peptide (CGRP) is expressed in visceral afferents and increased in TNBS colitis. This study used antibodies to nerve growth factor (NGF), brain derived nerve growth factor (BDNF), and antagonists to CGRP to examine their role in visceral hypersensitivity. TNBS induced a visceral hypersensitivity which was blocked by BDNF antibodies and mimicked in a dose-dependent fashion by intraperitonally injected BDNF. This hypersensitivity could be inhibited by a CGRP antagonist, leading the authors to conclude that both NGF and BDNF are key mediators of hyperalgesic effect of inflammation and act through CGRP as a final common pathway.
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Effect of exogenous brain derived neurotrophic factor (BDNF) (0–100 ng/rat in 0.1% bovine serum albumin (BSA), intraperitoneally (IP)) on colonic reaction threshold of rats in response to …