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논문 기본 정보

자료유형
학술저널
저자정보
Ma, Yuan (Research Institute of Veterinary Medicine, Chungbuk National University) Ma, Hong (College of Pharmacy, Chungbuk National University) Jo, Young-Jun (College of Pharmacy, Chungbuk National University) Kim, Dong-Seon (UniGen, Inc) Woo, Sung-Sick (UniGen, Inc) Li, Rihua (College of Pharmacy, Woosuk University) Hong, Jin-Tae (College of Pharmacy, Chungbuk National University) Moon, Dong-Cheul (College of Pharmacy, Chungbuk National University) Oh, Ki-Wan (College of Pharmacy, Chungbuk National University) Eun, Jae-Soon (College of Pharmacy, Woosuk University)
저널정보
한국응용약물학회 Biomolecules & Therapeutics(구 응용약물학회지) Biomolecules & therapeutics 제16권 제4호
발행연도
2008.1
수록면
328 - 335 (8page)

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This study was undertaken to investigate whether honokiol could enhance the pentobarbitalinduced sleeping behaviors through $\gamma$-aminobutyric acid (GABA) receptor $Cl^-$ channel activation. Thirty minutes after the oral administration of honokiol, mice were received sodium pentobarbital (42 mg/kg, i.p.). The time elapsed from pentobarbital injection to the loss of the righting reflex was taken as sleeping latency. The time elapsed between the loss and voluntary recovery of the righting reflex was considered as the total sleeping time. Western blot technique and $Cl^-$ sensitive fluorescence probe were used to detect the expression of $GABA_A$ receptor subunits and $Cl^-$ influx in the primary cultured cerebellar granule cells. Honokiol (0.1 and 0.2 mg/kg) prolonged the sleeping time induced by pentobarbital (42 mg/kg) in a dosage-dependent manner. Honokiol (20 and 50 ${\mu}M$) increased $Cl^-$ influx in primary cultured cerebellar granule cells, and selectively increased the $GABA_A$ receptor $\alpha$-subunit expression, but had no effect on the abundance of $\beta$ or $\gamma$-subunits. Chronic treatment with 20 ${\mu}M$ honokiol in primary cultured cerebellar neurons did not affect the abundance of GAD65/67. The results suggested that honokiol could potentiate pentobarbital-induced sleeping through $GABA_A$ receptor $Cl^-$ channel activation.

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