| Project/Area Number |
16614009
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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 |
睡眠学
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| Research Institution | Fukushima Medical University |
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Principal Investigator |
KAYAMA Yukihiko Fukushima Med.Univ., Dept.Physiol., Professor, 医学部, 教授 (30035224)
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| Co-Investigator(Kenkyū-buntansha) |
KOYAMA Yoshimasa Fukushima Univ., Dept.Sci.Tchnol., Professor, 共生システム理工学類, 教授 (80183812)
高橋 和巳 福島県立医科大学, 医学部, 助手 (90325952)
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| Project Period (FY) |
2004 – 2005
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| Project Status |
Completed (Fiscal Year 2005)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,900,000)
Fiscal Year 2005: ¥1,200,000 (Direct Cost: ¥1,200,000)
Fiscal Year 2004: ¥2,700,000 (Direct Cost: ¥2,700,000)
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| Keywords | orexin / acetylcholine / pedunculopontine tegmental / substantia nigra / serotonin / laterodorsal tegmental nucleus / muscular atonia / GABA / アセチルコリンニューロン / セロトニンニューロン / 筋トーヌス / ノルアドレナリンニューロン / 外側視床下部 / 青斑核 / ニューロバイオチン |
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| Research Abstract |
To elucidate the orexinergic mechanisms that regulate wakefulness or narcolepsy effects of orexin on muscular tonus in decerebrated cats were examined
1.Electrical stimulation to the pedunculopontine tegmental nucleus (PPT) induced muscular atonia.
2.Injection of orexin to the PPT close to the stimulated site suppressed the muscular atonia induced by the PPT stimulation.
3.Injection of orexin to the substantia nigra pars reticulata (SNr) induced the same ationia-suppressing effect.
4.Effect of orexin was blocked by the subsequence injection of bicuculline, GABAA antagonist
Microdialysis study in free moving rat revealed that orexin injected in the PPT increased the release of GABA from the PPT.
Unit recording study revealed that orexin, when applied directly to the PPT, caused excitatory influence on the brainstem cholinergic neurons. When large amount of orexin was applied to wide area around the neurons, the activity of the neurons were strongly suppressed for a long time.
These results suggest that orexin suppressed the PPN-induced muscular atonia through activation of GABAergic interneurons in the PPT or the terminals of GABAergic afferents from the SNr.
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