Document Detail


Ginsenoside Rg1 promotes glutamate release via a calcium/calmodulin-dependent protein kinase II-dependent signaling pathway.
MedLine Citation:
PMID:  20381470     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Ginseng is one of most extensively used traditional oriental medicines worldwide with beneficial efficacy on cognitive function disorders. Pharmacological researches on its active ingredient--ginsenoside Rg1 revealed that it can improve learning and memory potentially via modulating neurotransmission in the central nervous system, whereas the specific mechanism involved has not been elucidated yet. Our previous studies have indicated that ginsenoside Rb1 could enhance glutamate release via PKA-dependent signaling pathway whereas Rg1 could enhance glutamate release via PKA-independent signaling pathway. In this work we sought to determine the role of another key mediator in neurotransmitter release--calcium/calmodulin-dependent protein kinase II (CaMKII) in the mechanism of Rg1-enhanced glutamate release. Pre-treatment with CaMKII inhibitor KN93 blocked Rg1-induced glutamate release in primary hippocampal neurons. To investigate how CaMKII was involved in this process, the effect of Rg1 on CaMKII was further studied. Rg1 activated CaMKII and subsequently increased phosphorylation level of Synapsin I (Serine(603), a substrate site of CaMKII)--an abundant phosphoprotein essential for regulating neurotransmitter release, which could be blocked by pre-treatment with CaMKII inhibitor KN93. In conclusion, the present study suggests that Rg1 promotes glutamate release potentially via a CaMKII-dependent signaling pathway in which Synapsin I may potentially act as a downstream effector. Combined with our previous study on Rb1, these two studies altogether indicated that different ginsenosides may promote neurotransmitter release via differential signaling pathways.
Authors:
Zhi-Jun Liu; Ming Zhao; Yun Zhang; Jian-Fei Xue; Nai-Hong Chen
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-04-08
Journal Detail:
Title:  Brain research     Volume:  1333     ISSN:  1872-6240     ISO Abbreviation:  Brain Res.     Publication Date:  2010 May 
Date Detail:
Created Date:  2010-05-17     Completed Date:  2010-08-12     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  0045503     Medline TA:  Brain Res     Country:  Netherlands    
Other Details:
Languages:  eng     Pagination:  1-8     Citation Subset:  IM    
Copyright Information:
2010 Elsevier B.V. All rights reserved.
Affiliation:
Institute of Material Medica, Chinese Academy of Medical Sciences and Peking Union Medical College (Key Laboratory of Bioactive Substances and Resources Utilization, Ministry of Education), Beijing, People's Republic of China 100050.
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Animals
Benzylamines / pharmacology
Calcium-Calmodulin-Dependent Protein Kinase Type 2 / metabolism*
Cells, Cultured
Central Nervous System Agents / chemistry,  pharmacology*
Dose-Response Relationship, Drug
Down-Regulation / drug effects
Embryo, Mammalian
Ginsenosides / chemistry,  pharmacology*
Glutamic Acid / metabolism*
Hippocampus / cytology
Mice
Mice, Inbred C57BL
Neurons / drug effects*
Phosphorylation / drug effects
Protein Kinase Inhibitors / pharmacology
Serine / genetics
Signal Transduction / drug effects*
Sulfonamides / pharmacology
Synapsins / metabolism
Chemical
Reg. No./Substance:
0/Benzylamines; 0/Central Nervous System Agents; 0/Ginsenosides; 0/Protein Kinase Inhibitors; 0/Sulfonamides; 0/Synapsins; 139298-40-1/KN 93; 22427-39-0/ginsenoside Rg1; 56-45-1/Serine; 56-86-0/Glutamic Acid; EC 2.7.11.17/Calcium-Calmodulin-Dependent Protein Kinase Type 2

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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