| Co-Investigator(Kenkyū-buntansha) |
OZAKI Noriyuki Fukushima Medical University, School of Medicine, Department of anatomy, Assistant, 医学部, 助手 (40244371)
TONOSAKI Yoshikazu Fukushima Medical University, School of Medicine, Department of anatomy, Assistant, 医学部, 助手 (50155545)
SUGIURA Yasuo Fukushima Medical University, School of Medicine, Department of anatomy, Professor, 医学部, 教授 (50093042)
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| Research Abstract |
Chronic pain like causalgia, phantom pain, and reflex sympathetic dystrophy, is caused by peripheral nerve injury. Pain mechanisms of these syndromes were still not clear, in spite of many hypotheses. Sato and Perl (Science, 1991) reported that peripheral nerve injury induces an adrenergic excitability in normal C-fiber nociceptors that is mediated through an adrenergic receptor(AR) with α2 pharmacological characteristics. The present research examined the effects of injury to limb nerves (sciatic or tibial) or the lumbar sympathetic trunk(SYX) on changes of expression of α2-AR in the dorsal root ganglion(DRG), changes of responsiveness to noradrenalin treatment, and determination of possible expression of α2-AR subtypes. These projects showed the results below. (1) The DRG neurons, mainly small size cells increased the binding of clonidine, α2-AR agonist, by nerve injuries and SYX. (2) Following noradrenaline injection into the plantar subcutis suffered SYX, Fos protein expression as a marker of activated neurons augmented in the spinal dorsal horn, especially laminae I and II. This phenomenon may be induced by increased nociceptive inputs from DRG neurons activated by SYX . A stimulant of the C-fiber,capsaicin also showed the enhanced responsiveness by SYX. (3) The increased expression of α2-AR subtypes was showed in α2C subtype, using in situ hybridization with oligoprobes coding mRNAs of α2-AR subtypes, α2A and α2C. The expression of trk receptors also showed increase of trkC only by SYX. These results suggested that peripheral nerve injury including the sympathetic nerve may cause hyperalgesia due to the increased expression of the α2-AR in the DRG neuron.
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