title: Changes in phosphorylation of ERK and Fos expression in dorsal horn neurons following noxious stimulation in a rat model of neuritis of the nerve root.
abstract: Mechanical compression and chemical inflammation of the spinal nerve root are considered major sensory pathologies secondary to a lumbar disc herniation. In order to elucidate the dorsal horn responsiveness to noxious stimulation to the peripheral tissue in the neuritis model of the nerve root, we examined extracellular signal-regulated kinase (ERK) phosphorylation and Fos expression in spinal cord dorsal horn neurons. Male Sprague-Dawley rats received hemilaminectomies and the implantation of disc tissue that was obtained from coccygeal intervertebral discs. Three or 7 days after surgery, rats were perfused after receiving noxious mechanical stimulation of the plantar surface of the hind paw using a hemoclip, and the L4/5 spinal cord was processed for immunohistochemistry with antibodies for phospho-ERK and Fos. The number of Fos-immunoreactive (Fos-LI) neurons and phospho-ERK-immunoreactive (phospho-ERK-LI) neurons in the neuritis group after the noxious stimulation significantly increased compared to the sham-treated group at 3 and 7 days after surgery. The change in number of phospho-ERK-LI and Fos-LI neurons occurred mainly in the superficial dorsal horn. The number of Fos-LI neurons observed when the MEK inhibitor, U0126, was administered was significantly suppressed compared to the DMSO- (vehicle control) administered group. The increase in ERK phosphorylation and Fos expression in the spinal cord dorsal horn neurons indicates that responses/activation by the noxious stimulation applied to the periphery were elevated in spinal cord neurons in this neuritis model of the lumbar nerve root. Moreover, the increase in the Fos expression in the spinal cord dorsal horn may have been the result of the activation of the MAP kinase cascade.
authors.affiliation: Department of Anatomy and Neuroscience, Hyogo College of Medicine, 1-1 Mukogawa-cho, Nishinomiya, Japan.
authors.forename: Yutaka
authors.initials: Y
authors.lastname: Kominato
authors.forename: Toshiya
authors.initials: T
authors.lastname: Tachibana
authors.forename: Yi
authors.initials: Y
authors.lastname: Dai
authors.forename: Hiroaki
authors.initials: H
authors.lastname: Tsujino
authors.forename: Souji
authors.initials: S
authors.lastname: Maruo
authors.forename: Koichi
authors.initials: K
authors.lastname: Noguchi
mesh_terms: D000818:Animals; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005786:Gene Expression Regulation / Q000187:drug effects / Q000502:physiology; D008297:Male; D020928:Mitogen-Activated Protein Kinases / Q000037:antagonists & inhibitors / Q000096:biosynthesis*; D009443:Neuritis / Q000378:metabolism*; D010766:Phosphorylation / Q000187:drug effects; D010812:Physical Stimulation / Q000009:adverse effects / Q000379:methods; D020671:Posterior Horn Cells / Q000187:drug effects / Q000378:metabolism*; D016760:Proto-Oncogene Proteins c-fos / Q000096:biosynthesis*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013126:Spinal Nerve Roots / Q000187:drug effects / Q000378:metabolism*
chemical_list: D004791:Enzyme Inhibitors; D016760:Proto-Oncogene Proteins c-fos; D020928:Mitogen-Activated Protein Kinases