2006 Fiscal Year Final Research Report Summary
Effects of alpha 2 adrenoceptors or opioid receptors on spinal analgesia
| Project/Area Number |
15390470
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| Research Category |
Grant-in-Aid for Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Anesthesiology/Resuscitation studies
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| Research Institution | The University of Tokyo |
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Principal Investigator |
SEKIYAMA Hiroshi The University of Tokyo, Hospital, Assistant professor (40301105)
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| Co-Investigator(Kenkyū-buntansha) |
HANAOKA Kazuo The University of Tokyo, JR Tokyo General Hospital, Hospital director (80010403)
TAGAMI Megumi The University of Tokyo, Toho medical Sakura Center, Professor (90107657)
KITAMURA Takayuki The University of Tokyo, Hospital, Assistant professor (50302609)
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| Project Period (FY) |
2003 – 2006
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| Keywords | clonidine / dexmedetomidine / analgesia / antipruritic effect |
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| Research Abstract |
In rat models of neuropathic pain, inflammatory pain, and postoperative pain, we evaluated effects of clonidine cream, topically applied onto the plantar surface of the injured or uninjured paw, on thermal hyperalgesia and mechanical allodynia to von Frey filaments. Topical clonidine cream in concentrations examined significantly reduced hypersensitivity and lumbar spinal Fos-like immunoreactivity in rats with neuropathic pain, probably through activation of peripherally located alpha2 adrenoceptors.
Alpha_2-adrenergic agonists have been used extensively to treat patients with hypertension, abuse of drugs or chronic pain. However, antipruritic effects of alpha_2-receptors adrenoceptor agonist is not well known. The purpose of this study is to examine the effects of dexmedetomidine on the scratching behavior and spinal c-Fos expression, using the mouse pruritogen-induced scratching model. Dexmedetomidine has antipruritic activity which is mediated by alpha_2-receptors and reduces compound 48/80 induced spinal c-Fos expression in mice. It may be useful to use dexmedetomidine to treat pruritus. In a mouse puritoceptive itch model, systemic DEX produces a significant antipruritic effect primarily by activating alpha2A-adrenoceptors in the spinal cord.
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