Changes in trkA expression in the dorsal root ganglion after peripheral nerve injury.
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 peripheral nerve injury. The present study examined changes of TrkA immunoreactivity and trkA mRNA expression in the DRG after segmental nerve ligation. In the normal L5 DRG of the rat, there were, on average, 4700 TrkA-immunoreactive (TrkA-IR) neurons, representing 42% of the total neuronal population. Following L5 spinal nerve ligation, the number of TrkA-IR neurons in the L5 DRG slowly declined, reducing by 25% at 1 week and 35% at 3 weeks postoperation (PO). In contrast, trkA mRNA in these ganglia showed a significant decrease from 3 days to 3 weeks PO and was followed by a full recovery at 2 months PO. The early decrease of trkA mRNA is likely due to deprivation of target-derived NGF, which is caused by nerve ligation, and the recovery might be because substitute sources of NGF become available. Despite the decline in trkA mRNA in the ganglion, 3000 injured DRG neurons sustain TrkA immunoreactivity, suggesting that exogenous NGF can still influence these TrkA expressing neurons, even though they are isolated from the periphery. Accordingly, the effects of endogenous NGF should be as well manifested by local administration of NGF to the ganglion as to the stump of the damaged nerve.
Shen
H
H
Marine Biomedical Institute, University of Texas Medical Branch, Galveston 77555-1069, USA.
Chung
J M
JM
Coggeshall
R E
RE
Chung
K
K
D000818:Animals; D002452:Cell Count; D048429:Cell Size; D005727:Ganglia, Spinal / Q000378:metabolism* / Q000473:pathology; D007150:Immunohistochemistry; D008026:Ligation; D008161:Lumbosacral Region; D008297:Male; D009474:Neurons / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020917:Receptor, trkA / Q000235:genetics / Q000378:metabolism*; D013127:Spinal Nerves / Q000293:injuries*; D014949:Wounds, Nonpenetrating / Q000378:metabolism* / Q000473:pathology
D012333:RNA, Messenger; D020917:Receptor, trkA