Sedative-Hypnotic and Receptor Binding Studies of Fermented Marine Organisms

Joung, Hye Young; Kang, Young Mi; Lee, Bae Jin; Chung, Sun Yong; Kim, Kyung Soo; Shim, Insop

doi:10.4062/biomolther.2014.122

Cited by 3 publications

(1 citation statement)

References 19 publications

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“…In our experiment, quinpirole affected the pentobarbital-sleep onset time, but not the MT-sleep onset time. Because quinpirole as a D2-like receptor agonist produces a sedative effect related to GABA receptor modulation ( Canales and Iversen, 2000 ; Joung et al ., 2015 ), quinpirole may indirectly affect pentobarbital-induced sleep. However, in this study, quinpirole did not modulate the sleep onset time in MT-administered mice.…”

Section: Discussionmentioning

confidence: 99%

Quinpirole Increases Melatonin-Augmented Pentobarbital Sleep via Cortical ERK, p38 MAPK, and PKC in Mice

Hong

Kwon

Hwang

et al. 2016

Biomolecules & Therapeutics

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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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Section: Discussionmentioning

confidence: 99%

Quinpirole Increases Melatonin-Augmented Pentobarbital Sleep via Cortical ERK, p38 MAPK, and PKC in Mice

Hong

Kwon

Hwang

et al. 2016

Biomolecules & Therapeutics

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Screening Methods for the Evaluation of Sedative-Hypnotics

Jose

Lakshmanan

2022

Introduction to Basics of Pharmacology and Toxicology

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Sedative–Hypnotic Activity of the Water Extracts of Coptidis Rhizoma in Rodents

Joung

Lee

et al. 2022

Clocks & Sleep

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Many medicinal plants have been used in Asia for treating a variety of mental diseases, including insomnia and depression. However, their sedative–hypnotic effects and mechanisms have not been clarified yet. Accordingly, the objective of this study was to investigate the sedative–hypnotic effects of water extracts of five medicinal plants: Coptidis Rhizoma, Lycii Fructus, Angelicae sinensis Radix, Bupleuri Radix, and Polygonum multiflorum Thunberg. The binding abilities of five medicinal plant extracts to the GABAA–BZD and 5-HT2C receptors were compared. Their abilities to activate arylalkylamine N-acetyltransferase (AANAT), a melatonin synthesis enzyme, in pineal cells were also determined. Following in vitro tests, the sedative and hypnotic activities of extracts with the highest activities were determined in an animal sleep model. In the binding assay, the water extracts of Coptidis Rhizoma (WCR) showed high binding affinity to the GABAA–BZD and 5-HT2C receptors in a dose-dependent manner. Additionally, WCR increased the AANAT activity up to five times compared with the baseline level. Further animal sleep model experiments showed that WCR potentiated pentobarbital-induced sleep by prolonging the sleep time. It also decreased the sleep onset time in mice. In addition, WCR reduced wake time and increased non-rapid eye movement (NREM) sleep without EEG power density (percentages of δ, θ, and α waves) during NREM sleep in rats. WCR could effectively induce NREM sleep without altering the architectural physiologic profile of sleep. This is the first report of the sedative–hypnotic effect of Coptidis Rhizoma possibly by regulating GABAA and 5-HT2C receptors and by activating AANAT activity.

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Sedative-Hypnotic and Receptor Binding Studies of Fermented Marine Organisms

Cited by 3 publications

References 19 publications

Quinpirole Increases Melatonin-Augmented Pentobarbital Sleep via Cortical ERK, p38 MAPK, and PKC in Mice

Quinpirole Increases Melatonin-Augmented Pentobarbital Sleep via Cortical ERK, p38 MAPK, and PKC in Mice

Screening Methods for the Evaluation of Sedative-Hypnotics

Sedative–Hypnotic Activity of the Water Extracts of Coptidis Rhizoma in Rodents

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