The hypothesis that nerve growth factor (NGF) and brain-derived neurotrophi
c factor (BDNF) contribute to hyperalgesia resulting from nerve damage was
tested in rats in which the sciatic nerve was partially transected on one s
ide. Administration of antisera raised against NGF and BDNF relieved mechan
ical and thermal hyperalgesia in these animals. It has been suggested that
NGF may elicit hyperalgesia by inducing mast cells to release algesic agent
s such as serotonin (5-HT). We found that degranulation of mast cells with
compound 48/80 relieved mechanical and thermal hyperalgesia produced by ner
ve damage. We also found that local injection of the 5-HT2A and 5-HT3 recep
tor antagonists ketanserin and ICS 205-930 into the affected hind paw relie
ved mechanical hyperalgesia in a dose-dependent fashion. These findings sup
port the idea that in this rat model of hyperalgesia due to peripheral nerv
e damage, NGF acts on mast cells to induce release of 5-HT, which sensitize
s nociceptors. Hyperalgesia due to nerve injury and hyperalgesia due to inf
lammation may share some common features. (C) 1999 International Associatio
n for the Study of Pain. Published by Elsevier Science B.V.