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Salvia miltiorrhiza Bunge Blocks Ethanol-Induced Synaptic Dysfunction through Regulation of NMDA Receptor-Dependent Synaptic Transmission.

Park HJ, Lee S, Jung JW, Lee YC, Choi SM, Kim DH - Biomol Ther (Seoul) (2016)

Bottom Line: In this test, ethanol (1 g/kg, i.p.) impaired object recognition memory, but SM (200 mg/kg) prevented this impairment.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicinal Biotechnology, College of Health Sciences and Institute of Convergence Bio-Health, Dong-A University, Busan 49315, Republic of Korea.

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.

No MeSH data available.


Related in: MedlinePlus

SM rescues ethanol-induced decrease of fEPSPNMDAR. To isolate fEPSPNMDAR, NBQX (50 μM) was perfused during recording. The peak of the evoked field potential responses were averaged from four consecutive recordings (EPSPs) evoked at 30 s intervals (Ampk). (A) The effect of SM on fEPSPNMDAR. (B) SM reduced ethanol-induced decrease of fEPSPNMDAR in a concentration dependent manner. Data were normalized to baseline (0–20 min) and represent mean ± S.E.M. EtOH, ethanol. SM, Salvia miltiorrhiza extract.
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f2-bt-24-433: SM rescues ethanol-induced decrease of fEPSPNMDAR. To isolate fEPSPNMDAR, NBQX (50 μM) was perfused during recording. The peak of the evoked field potential responses were averaged from four consecutive recordings (EPSPs) evoked at 30 s intervals (Ampk). (A) The effect of SM on fEPSPNMDAR. (B) SM reduced ethanol-induced decrease of fEPSPNMDAR in a concentration dependent manner. Data were normalized to baseline (0–20 min) and represent mean ± S.E.M. EtOH, ethanol. SM, Salvia miltiorrhiza extract.

Mentions: Previous reports have suggested that ethanol impairs hippocampal NMDAR-mediated fEPSP (fEPSPNMDAR), and this may be a mechanism of ethanol-induced memory impairment (Hicklin et al., 2011). Therefore, we tested the effect of SM on ethanol-induced NMDAR fEPSP (fEPSPNMDAR) impairment in the hippocampus. To isolate fEPSPNMDAR, we perfused NBQX (50 μM) (Alvestad et al., 2003), an AMPAR antagonist. SM itself did not affect fEPSPNMDAR (Fig. 2A). Ethanol (80 mM) reduced fEPSPNMDAR, but SM blocked this in a concentration-dependent manner (Fig. 2B).


Salvia miltiorrhiza Bunge Blocks Ethanol-Induced Synaptic Dysfunction through Regulation of NMDA Receptor-Dependent Synaptic Transmission.

Park HJ, Lee S, Jung JW, Lee YC, Choi SM, Kim DH - Biomol Ther (Seoul) (2016)

SM rescues ethanol-induced decrease of fEPSPNMDAR. To isolate fEPSPNMDAR, NBQX (50 μM) was perfused during recording. The peak of the evoked field potential responses were averaged from four consecutive recordings (EPSPs) evoked at 30 s intervals (Ampk). (A) The effect of SM on fEPSPNMDAR. (B) SM reduced ethanol-induced decrease of fEPSPNMDAR in a concentration dependent manner. Data were normalized to baseline (0–20 min) and represent mean ± S.E.M. EtOH, ethanol. SM, Salvia miltiorrhiza extract.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4930288&req=5

f2-bt-24-433: SM rescues ethanol-induced decrease of fEPSPNMDAR. To isolate fEPSPNMDAR, NBQX (50 μM) was perfused during recording. The peak of the evoked field potential responses were averaged from four consecutive recordings (EPSPs) evoked at 30 s intervals (Ampk). (A) The effect of SM on fEPSPNMDAR. (B) SM reduced ethanol-induced decrease of fEPSPNMDAR in a concentration dependent manner. Data were normalized to baseline (0–20 min) and represent mean ± S.E.M. EtOH, ethanol. SM, Salvia miltiorrhiza extract.
Mentions: Previous reports have suggested that ethanol impairs hippocampal NMDAR-mediated fEPSP (fEPSPNMDAR), and this may be a mechanism of ethanol-induced memory impairment (Hicklin et al., 2011). Therefore, we tested the effect of SM on ethanol-induced NMDAR fEPSP (fEPSPNMDAR) impairment in the hippocampus. To isolate fEPSPNMDAR, we perfused NBQX (50 μM) (Alvestad et al., 2003), an AMPAR antagonist. SM itself did not affect fEPSPNMDAR (Fig. 2A). Ethanol (80 mM) reduced fEPSPNMDAR, but SM blocked this in a concentration-dependent manner (Fig. 2B).

Bottom Line: In this test, ethanol (1 g/kg, i.p.) impaired object recognition memory, but SM (200 mg/kg) prevented this impairment.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.

View Article: PubMed Central - PubMed

Affiliation: Department of Medicinal Biotechnology, College of Health Sciences and Institute of Convergence Bio-Health, Dong-A University, Busan 49315, Republic of Korea.

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.

No MeSH data available.


Related in: MedlinePlus