Most of the biological effects of nerve growth factor (NGF) are mediated by
TrkA, the high affinity receptor for NGF. Previous studies have shown that
NGF levels in the dorsal root ganglia (DRG) fluctuate following a peripher
al nerve injury. The present study examined changes of TrkA immunoreactivit
y and trkA mRNA expression in the DRG after segmental nerve ligation. In th
e normal L5 DRG of the rat, there were, on average, 4700 TrkA-immunoreactiv
e (TrkA-IR) neurons, representing 42% of the total neuronal population. Fol
lowing L5 spinal nerve ligation, the number of TrkA-IR neurons in the L5 DR
G slowly declined, reducing by 25% at 1 week and 35% at 3 weeks postoperati
on (PO). In contrast, trkA mRNA in these ganglia showed a significant decre
ase from 3 days to 3 weeks PO and was followed by a full recovery at 2 mont
hs PO. The early decrease of trkA mRNA is likely due to deprivation of targ
et-derived NGF, which is caused by nerve ligation, and the recovery might b
e because substitute sources of NGF become available. Despite the decline i
n trkA mRNA in the ganglion, 3000 injured DRG neurons sustain TrkA immunore
activity, suggesting that exogenous NGF can still influence these TrkA expr
essing neurons, even though they are isolated from the periphery. According
ly, the effects of endogenous NGF should be as well manifested by local adm
inistration of NGF to the ganglion as to the stump of the damaged nerve.