Endogenous nerve growth factor increases the sensitivity to bradykinin in small dorsal root ganglion neurons of adjuvant inflamed rats.

To examine the cellular mechanisms of hyperalgesia observed in an adjuvant-induced chronic inflammation, the role of nerve growth factor (NGF) in the response to bradykinin (BK) in small neurons from dorsal root ganglia (DRG) was studied via intracellular recordings. After 2 days of cultivation in the absence of NGF, the percentage of neurons from adjuvant-inflamed (AI) rats which were depolarized by BK (53%) was significantly higher than that in neurons from intact rats (13%). This higher percentage in AI rat neurons was significantly reduced after culturing with anti-NGF (17%), but was not influenced by the addition of NGF (57%). The present result demonstrated that sensitivity to BK of DRG neurons from AI rats is increased due to the action of endogenous NGF, suggesting that plastic change in primary afferent neurons caused by NGF may be one of the mechanisms involved in hyperalgesia.