Single unit recording of immunohistcchemically identified hypothalamic sleep waking-promoting neurons
| Project/Area Number |
18603006
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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 |
TAKAHASHI Kazumi Fukushima Medical University, Department of Neurophysiology, Lecturer (90325952)
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| Co-Investigator(Kenkyū-buntansha) |
KAYAMA Yukihiko Fukushima Medical Univensity, 医学部, professor (30035224)
KOYAMA Yoshimasa Fukushima University, Faculty of Symbiotic Systems Science, professor (80183812)
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| Project Period (FY) |
2006 – 2007
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| Project Status |
Completed (Fiscal Year 2007)
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| Budget Amount *help |
¥4,020,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥420,000)
Fiscal Year 2007: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2006: ¥2,200,000 (Direct Cost: ¥2,200,000)
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| Keywords | mouse / unanesthetized animal / single unit activity / hypothalamus / histamine / sleep / EEG / orexin / 睡眠・覚醒調節 / ニューロバイオチン |
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| Research Abstract |
We recorded spontaneous activity of immunohistochemically identified hypothalamic neurons during sleep-waking cycles in the head-restrained unanesthetized mice. The tuberomammillary histaminergic neuronwave sleep to waking, the displayed firing exclusively during wakefulness and the firing rate varied in the different waking states, being lowest during quiet waking, moderate during active waking and highest during attentive waking elicited by touching the tail. Sleep-specific neurons were recorded in the preoptic area (POA). At the transition from waking to drowsy state, POA sleep : specific neurons began firing either at the onset or after the onset of EEG synchronization, the EEG sign of sleep, while histaminergic neurons stopped discharging clearly before the onset of EEG synchronization. At the transition from slow-wave sleep to waking, the POA sleep-specific neurons stopped firing prior to the onset of EEG desynchronization, while histaminergic neurons started firing with a long d
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elay after the EEG change. The lateral hypothalamic orexinergic neuron showed waking-active property, starting discharge prior to the -onset of EEG desynchronization and histaminergic activity, and ceased their firing shortly after the onset of EEG synchronization. At the transition from paradoxical sleep to wakefulness, the onset of orexinergic activity preceded the return of muscle tonus. These results suggest that 1) the activity of histaminergic neurons is maintained through orexinergic excitation and involved in maintenance of a higher level of vigilance, 2) histaminergic activity during behavioral states is not controlled exclusively by POA sleep-promoting neurons, 3) the activity of orexinergic neuron plays an important wake-promoting role and antagonizes cortical deactivation and loss of muscle tone. The present results also provide consistent explanation to the well-known phenomenon that anti-histaminergic drugs cause sleepiness. Unfortunately, we could not try direct application of pharmacological agents to the neuron to elucidate the regulation mechanisms underlying each neuronal activity, but we could obtain meaningful finding and largely advance investigation of neuronal mechanisms of sleep-waking regulation. Less
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Report
(3 results)
Research Products
(18 results)
