Neurotrophins mediate specific effects on sensory neurons through tyrosine kinase receptors. Most of these neurons also co-express the neurotrophin receptor p75 (p75(NTR)), but it, function has remained obscure. We now show that nerve growth factor but not brain-derived neurotrophic factor or neurotrophin-3 selectively increases the expression of bradykinin binding sites on cultured dorsal root ganglion neurons from adult mouse via p75(NTR). This up-regulation of bradykinin binding sites did not occur in neurons from mice lacking p75(NTR) Or in neurons from wild-type mice treated with p75(NTR)-blocking antibody, indicating that tyrosine kinase receptors alone are not sufficient to trigger this physiological neuronal response. Thus, the interaction of nerve growth factor with p75(NTR) is an important factor contributing to chronic pain conditions. (C) 1997 IBRO. Published by Elsevier Science Ltd.