Biomolecules & Therapeutics

  • 제24권4호
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  • Pages.433-437
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  • 2016
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  • 1976-9148(pISSN)
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  • 2005-4483(eISSN)
한국응용약물학회 (The Korean Society of Applied Pharmacology)
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Salvia miltiorrhiza Bunge Blocks Ethanol-Induced Synaptic Dysfunction through Regulation of NMDA Receptor-Dependent Synaptic Transmission

  • Park, Hye Jin (Department of Medicinal Biotechnology, College of Health Sciences and Institute of Convergence Bio-Health, Dong-A University) ;
  • Lee, Seungheon (Department of Aquatic Biomedical Sciences, School of Marine Biomedical Science, College of Ocean Science, Jeju National University) ;
  • Jung, Ji Wook (Department of Herbal Medicinal Pharmacology, College of Herbal Bio-industry, Daegu Haany University) ;
  • Lee, Young Choon (Department of Medicinal Biotechnology, College of Health Sciences and Institute of Convergence Bio-Health, Dong-A University) ;
  • Choi, Seong-Min (Department of Neurology, Chonnam National University Medical School) ;
  • Kim, Dong Hyun (Department of Medicinal Biotechnology, College of Health Sciences and Institute of Convergence Bio-Health, Dong-A University)
  • 투고 : 2015.11.24
  • 심사 : 2016.03.23
  • 발행 : 2016.07.01
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초록

Consumption of high doses of ethanol can lead to amnesia, which often manifests as a blackout. These blackouts experienced by ethanol consumers may be a major cause of the social problems associated with excess ethanol consumption. However, there is currently no established treatment for preventing these ethanol-induced blackouts. In this study, we tested the ethanol extract of the roots of Salvia miltiorrhiza (SM) for its ability to mitigate ethanol-induced behavioral and synaptic deficits. To test behavioral deficits, an object recognition test was conducted in mouse. In this test, ethanol (1 g/kg, i.p.) impaired object recognition memory, but SM (200 mg/kg) prevented this impairment. To evaluate synaptic deficits, NMDA receptor-mediated excitatory postsynaptic potential (EPSP) and long-term potentiation (LTP) in the mouse hippocampal slices were tested, as they are known to be vulnerable to ethanol and are associated with ethanol-induced amnesia. SM (10 and $100{\mu}g/ml$) significantly ameliorated ethanol-induced long-term potentiation and NMDA receptor-mediated EPSP deficits in the hippocampal slices. Therefore, these results suggest that SM prevents ethanol-induced amnesia by protecting the hippocampus from NMDA receptor-mediated synaptic transmission and synaptic plasticity deficits induced by ethanol.

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참고문헌

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