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논문 기본 정보

자료유형
학술저널
저자정보
Hong, Sa-Ik (Department of Pharmacology, School of Pharmacy, Sungkyunkwan University) Kwon, Seung-Hwan (Department of Pharmacology, School of Pharmacy, Sungkyunkwan University) Hwang, Ji-Young (Department of Pharmacology, School of Pharmacy, Sungkyunkwan University) Ma, Shi-Xun (Department of Pharmacology, School of Pharmacy, Sungkyunkwan University) Seo, Jee-Yeon (Department of Pharmacology, School of Pharmacy, Sungkyunkwan University) Ko, Yong-Hyun (Department of Pharmacology, School of Pharmacy, Sungkyunkwan University) Kim, Hyoung-Chun (Neurotoxicology Program, College of Pharmacy, Korea Institute of Drug Abuse, Kangwon National University) Lee, Seok-Yong (Department of Pharmacology, School of Pharmacy, Sungkyunkwan University) Jang, Choon-Gon (Department of Pharmacology, School of Pharmacy, Sungkyunkwan University)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제24권 제2호
발행연도
2016.1
수록면
115 - 122 (8page)

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Sleep, which is an essential part of human life, is modulated by neurotransmitter systems, including gamma-aminobutyric acid (GABA) and dopamine signaling. However, the mechanisms that initiate and maintain sleep remain obscure. In this study, we investigated the relationship between melatonin (MT) and dopamine D2-like receptor signaling in pentobarbital-induced sleep and the intracellular mechanisms of sleep maintenance in the cerebral cortex. In mice, pentobarbital-induced sleep was augmented by intraperitoneal administration of 30 mg/kg MT. To investigate the relationship between MT and D2-like receptors, we administered quinpirole, a D2-like receptor agonist, to MT- and pentobarbital-treated mice. Quinpirole (1 mg/kg, i.p.) increased the duration of MT-augmented sleep in mice. In addition, locomotor activity analysis showed that neither MT nor quinpirole produced sedative effects when administered alone. In order to understand the mechanisms underlying quinpirole-augmented sleep, we measured protein levels of mitogen-activated protein kinases (MAPKs) and cortical protein kinases related to MT signaling. Treatment with quinpirole or MT activated extracellular-signal-regulated kinase 1 and 2 (ERK1/2), p38 MAPK, and protein kinase C (PKC) in the cerebral cortex, while protein kinase A (PKA) activation was not altered significantly. Taken together, our results show that quinpirole increases the duration of MT-augmented sleep through ERK1/2, p38 MAPK, and PKC signaling. These findings suggest that modulation of D2-like receptors might enhance the effect of MT on sleep.

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