Glial cell line-derived neurotrophic factor normalizes neurochemical changes in injured dorsal root ganglion neurons and prevents the expression of experimental neuropathic pain.

摘要: Abstract Glial cell line-derived neurotrophic factor (GDNF) is necessary for the development of sensory neurons, and appears to be critical survival dorsal root ganglion (DRG) cells that bind lectin IB4. Intrathecal infusion GDNF has been shown prevent reverse behavioral expression experimental neuropathic pain arising from injury spinal nerves. This effect attributed a blockade voltage gated, tetrodotoxin-sensitive sodium channel subtype, NaV1.3, in injured DRG. Here we report given intrathecally via osmotic-pump nerve-injured rats (L5/L6 nerve ligation) prevented changes variety neurochemical markers DRG upon injury. They include loss binding IB4, downregulation purinergic receptor P2X3, upregulation galanin neuropeptide Y immunoreactivity large diameter cells, transcription ATF3. concomitantly ligation-induced tactile hypersensitivity thermal hyperalgesia. These observations suggest high dose, exogenous broad neuroprotective role primary afferent. The receptor(s) mediates these effects not known. GDNF's ability block states likely specific NaV1.3 expression.