• Hideo Doya, Seiji Ohtori, Kazuhisa Takahashi, Yasuchika Aoki, Hidetoshi Ino, Yuzuru Takahashi, Hideshige Moriya, and Toshihide Yamashita.
• Department of Orthopedic Surgery, Graduate School of Medicine, Chiba University, Chiba, Japan. dowya@graduate.chiba-u.jp
• Spine. 2005 Oct 15; 30 (20): 2252-6.

Study DesignWe investigated the extracellular signal-regulated kinase (ERK) activation by immunohistochemically detecting phosphorylated ERK (pERK) in the dorsal root ganglion (DRG) and spinal cord.ObjectiveTo clarify the ERK activation in the rat nervous system following DRG injury.Summary Of Background DataRadicular pain is known to be associated with DRG injury caused by intervertebral disc herniation. ERK is activated by phosphorylation in the DRG and spinal cord by noxious stimuli, which are related to pain hypersensitivity.MethodsFrom 2 minutes to 24 hours after the left L4 DRG crush injury, L4 DRGs and spinal cords were resected to prepare serial sections, which were investigated immunohistochemically.ResultsIn the DRG, ERK activation was detected in neurons and satellite cells at 2 minutes; the former was maintained at increased levels for 20 minutes, and the latter for 4 hours. At 30 minutes, pERK immunoreactivity was observed in Schwann cells, which continued for up to 24 hours. In the spinal cord, pERK-positive neurons were detected at 2 minutes, and the pERK levels were maintained at increased levels for 20 minutes.ConclusionsProfiles of pERK induction in neurons after DRG injury were similar between the DRG and spinal cord, whereas pERK induction in the satellite cells was more long lasting. The pERK induction in Schwann cells in the DRG was late onset and the most long lasting.

20 keywords...

hide…