| Project/Area Number |
15591613
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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 | HOKKAIDO UNIVERSITY |
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Principal Investigator |
HASHIMOTO Toshikazu Hokkaido Univ., Grad.School of Med., Inst., 大学院・医学研究科, 助手 (40281810)
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| Project Period (FY) |
2003 – 2004
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| Project Status |
Completed (Fiscal Year 2004)
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| Budget Amount *help |
¥2,700,000 (Direct Cost: ¥2,700,000)
Fiscal Year 2004: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2003: ¥1,500,000 (Direct Cost: ¥1,500,000)
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| Keywords | descending inhibitory pathway / nitrous oxide / c-Fos / locus coeruleus / GABA / corticotropin releasing factor / ノルエピネフリン産生細胞 / 脊髄 |
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| Research Abstract |
Recent studies have revealed that nitrous oxide activates noradrenergic neurons in the brain stem and GABAergic neurons in the spinal cord. However, the precise neuronal pathways that mediate these events remain to be determined.
In adult male Fischer rats, noradrenergic nuclei of the brain stem were selectively lesioned by intracerebroventricular application of anti-DssH-saporin. After that rats were exposed to nitrous oxide, and c-Fos immunostaining of GABAergic neurons was examined in the spinal cord. Fos immunoreactivity was diminished in the anti-DssH-saporin treated rats than control rats which were not destroyed noradrenergic nuclei. This result shows that noradrenergic nuclei of the brain stem are essential for nitrous oxide to activate GABAergic neurons in the spinal cord.
In the following study, adult male Fischer rats were administered α-helical CRH (a corticotropin releasing factor receptor antagonist), DAMGO (an opioid receptor agonist), and naloxne (an opioid receptor antagonist) intracerebroventricularly. Then they were exposed to nitrous oxide, and c-Fos immunoreactivity of brain stem noradrenergic nucleus (locus coeruleus) was examined. Diminishing of c-Fos immunoreactivity inα-helical CRH and naloxone administered rats suggests that both corticotropin releasing factor and opioid are involved in the activation of noradrenergic neurons in the brain stem.
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