Salvia miltiorrhiza Bunge Blocks Ethanol-Induced Synaptic Dysfunction through Regulation of NMDA Receptor-Dependent Synaptic Transmission.
10.4062/biomolther.2015.184
- Author:
Hye Jin PARK
1
;
Seungheon LEE
;
Ji Wook JUNG
;
Young Choon LEE
;
Seong Min CHOI
;
Dong Hyun KIM
Author Information
1. Department of Medicinal Biotechnology, College of Health Sciences and Institute of Convergence Bio-Health, Dong-A University, Busan 49315, Republic of Korea. drchoism@gmail.com
- Publication Type:Original Article
- Keywords:
Salvia miltiorrhiza;
Ethanol;
Synaptic plasticity;
NMDA receptor
- MeSH:
Amnesia;
Animals;
Ethanol;
Excitatory Postsynaptic Potentials;
Hippocampus;
Long-Term Potentiation;
Memory;
Mice;
N-Methylaspartate*;
Neuronal Plasticity;
Salvia miltiorrhiza*;
Salvia*;
Social Problems;
Synaptic Transmission*
- From:Biomolecules & Therapeutics
2016;24(4):433-437
- CountryRepublic of Korea
- Language:English
-
Abstract:
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 μg/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.
