| Budget Amount *help |
¥3,300,000 (Direct Cost: ¥3,300,000)
Fiscal Year 2003: ¥1,600,000 (Direct Cost: ¥1,600,000)
Fiscal Year 2002: ¥1,700,000 (Direct Cost: ¥1,700,000)
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| Research Abstract |
The head investigator of this research project and his coworkers found that N^6-nitro-L-arginine methyl ester (L-NAME), an inhibitor of nitric oxide synthase (NOS), increased REM sleep when administered to the diencephalon of a rat. On the other hand, NOC 12, a nitric oxide (NO) donor compound, decreased REM sleep when administered to the same region. Based on these and other results, we assumed that NO has a role in the diencephalon to regulate REM sleep. It might be further conceived that NO is involved in pathophysiology of altered consciousness and attentional disturbances. However, it is still obscure whether the REM sleep changes were attributed to quantitative changes in NO in the diencephalon or some other unknown effects of L-NAME and NOC 12. Therefore, we investigated in this project whether the level of NO in the diencephalon changes along with a circadian sleep-wake rhythm and whether L-NAME causes a decrease in the level of NO in the diencephalon. We performed surgical operation to rats to implant electrodes to record EEG, EMG and EOG (electrooculogram) and two microdialysis probes to measure the level of NO in the diencephalon and to administer L-NAME to the same region. After full recovery from the surgery for 1 week, electrodes and microdialysis probes of each rat were connected to respective equipments. The level of NO in the rat diencephalon indicated a circadian rhythm, high during night, active period of rats, and low during day when rats spend time sleeping. When L-NAME was administered to the diencephalon, the level of NO showed a decrease. Our results supported the hypothesis that NO in the diencephalon is involved in the regulation of REM sleep. It remains to be studied whether NO is also involved in pathophysiology of altered consciousness and attentional disturbances.
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