ArticlesHyperalgesia due to nerve damage: role of nerve growth factorTheodosiou, M.a; Rush, A. R.c; Zhou, F. X.c; Hu, D.a; Walker, S. J.b; Tracey, J. D.a,*Author Information aSchool of Anatomy, University of New South Wales, Sydney NSW 2052, Australia bSchool of Physiology and Pharmacology, University of New South Wales, Sydney NSW 2052, Australia cDepartment of Physiology, Flinders University, Adelaide SA 5001, Australia * Corresponding author. Tel.: +61-2-9385-2471; fax: +61-2-9313-6252. Received May 26, 1998; received in revised form December 4, 1998; accepted January 11, 1999 Pain: June 1, 1999 - Volume 81 - Issue 3 - p 245-255 doi: 10.1016/S0304-3959(99)00018-4 Buy Metrics Abstract The hypothesis that nerve growth factor (NGF) and brain-derived neurotrophic factor (BDNF) contribute to hyperalgesia resulting from nerve damage was tested in rats in which the sciatic nerve was partially transected on one side. Administration of antisera raised against NGF and BDNF relieved mechanical and thermal hyperalgesia in these animals. It has been suggested that NGF may elicit hyperalgesia by inducing mast cells to release algesic agents such as serotonin (5-HT). We found that degranulation of mast cells with compound 48/80 relieved mechanical and thermal hyperalgesia produced by nerve damage. We also found that local injection of the 5-HT2A and 5-HT3 receptor antagonists ketanserin and ICS 205-930 into the affected hind paw relieved mechanical hyperalgesia in a dose-dependent fashion. These findings support the idea that in this rat model of hyperalgesia due to peripheral nerve damage, NGF acts on mast cells to induce release of 5-HT, which sensitizes nociceptors. Hyperalgesia due to nerve injury and hyperalgesia due to inflammation may share some common features. © 1999 Lippincott Williams & Wilkins, Inc.