| Project/Area Number |
16591529
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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 |
Anesthesiology/Resuscitation studies
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| Research Institution | Niigata University |
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Principal Investigator |
SHIBUE Chieko Niigata University, Medical & Dental Hospital, Assistant, 医歯学総合病院, 助手 (90303148)
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| Co-Investigator(Kenkyū-buntansha) |
KOHNO Tatsuro Niigata University, Institute of Medicine and Dentistry, Associate Professor, 医歯学系, 助教授 (00313536)
HONMA Takayuki Niigata University, Institute of Medicine and Dentistry, Assistant, 医歯学系, 助手 (20345531)
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| Project Period (FY) |
2004 – 2006
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| Project Status |
Completed (Fiscal Year 2006)
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| Budget Amount *help |
¥3,500,000 (Direct Cost: ¥3,500,000)
Fiscal Year 2006: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 2005: ¥900,000 (Direct Cost: ¥900,000)
Fiscal Year 2004: ¥1,600,000 (Direct Cost: ¥1,600,000)
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| Keywords | inhaled anesthetics / dorsal horn / GABA / synaptic transmission |
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| Research Abstract |
Although isoflurane, a volatile anesthetic, can block the motor response to noxious stimulation (immobility and analgesia) and suppress autonomic responsiveness, how it exerts these effects at the neuronal level in the spinal cord is not fully understood. The effects of a clinically relevant concentration (1 rat minimum alveolar concentration) of isoflurane on electrically evoked and spontaneous excitatory/inhibitory transmission, and on the response to exogenous administration of the y-aminobutyric acid A-receptor agonist, muscimol, were examined in lamina II neurons of adult rat spinal cord slices using the whole-cell patch-clamp technique. The effect of isoflurane on the action potential-generating membrane property was also examined. Bath-applied isoflurane (1.5%, 1 rat minimum alveolar concentration) diminished dorsal root-evoked polysynaptic, but not monosynaptic excitatory postsynaptic currents. Glutamatergic miniature excitatory postsynaptic currents were also unaffected by isoflurane. In contrast, isoflurane prolonged the decay phase of evoked and miniature y-aminobutyric acid A receptor-mediated inhibitory postsynaptic currents, and increased the amplitude of the muscimol-induced current. Isoflurane had little effect on action potential discharge activity. Isoflurane augments y-aminobutyric acid mediated inhibitory transmission, leading to a decrease in the excitability of spinal dorsal horn neurons. This may be a possible mechanism for the antinociceptive effect of isoflurane in the spinal cord.
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