| Project/Area Number |
10671740
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Section | 一般 |
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| Research Field |
Functional basic dentistry
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| Research Institution | Hiroshima University |
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Principal Investigator |
IRIFUNE Masahiro University Dental Hospital, Anesthesiology, Hiroshima University, Associate Professor, 歯学部・附属病院, 助教授 (10176521)
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| Co-Investigator(Kenkyū-buntansha) |
DOHI Toshihiro Faculty of Dentistry, Pharmacology, Hiroshima University, Professor, 歯学部, 教授 (00034182)
KAWAHARA Michio University Dental Hospital, Anesthesiology, Hiroshima University, Professor, 歯学部・附属病院, 教授 (30034094)
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| Project Period (FY) |
1998 – 1999
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| Project Status |
Completed (Fiscal Year 1999)
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| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 1999: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1998: ¥2,800,000 (Direct Cost: ¥2,800,000)
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| Keywords | GABAィイD2AィエD2 receptors / Excitatory amino acid receptors / Muscimol / Bicuculline / L-Allyglycine / N-methyl-D-aspartate / Kainic aci / General anesthetics / 全身麻酔 / GABA神経 / 正向反射 / プロポフォール / マイクロダイアリシス |
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| Research Abstract |
We examined the potentiation of GABAィイD2AィエD2 receptor function by the intravenous anesthetics. propofol and ketamine, using a behavioral model in adult male ddY mice. General anesthetic potencies were evaluated by a rating scale for righting reflex. All drugs were administered intraperitoneally. The GABAィイD2AィエD2 receptor agonist muscimol potentiated propofol-induced anesthesia in a dose-dependent fashion. The GABAィイD2AィエD2 receptor antagonist bicuculline dose-dependently antagonized propofol anesthesia. The excitatory amino acid (EAA) receptor agonists. NMDA and kainic acid, failed to reverse the anesthetic action of propofol. Similarly, muscimol potentiated and bicuculline inhibited ketamine-induced anesthesia. The GABA synthesis inhibitor L-allylglycine that depletes GABA from presynaptic nerve terminals did not affect ketamine anesthesia. However, an NMDA receptor agonist antagonized and antagonists potentiated ketamine anesthesia. These results suggest that propofol anesthesia is mediated by GABAィイD2AィエD2 receptors, not by EAA receptors, and that ketamine anesthesia is mediated by both GABAィイD2AィエD2 and NMDA receptors.
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