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Effects and wavelet spectral entropy analysis of rhubarb extracts rhein on synaptic transmission in rat hippocampal ca1 area in vitro

摘要:

Background 5-dihydroxyanthraquinone-2-carboxylic acid (rhein) inhibits oxidoreduction induced by reducing nicotingamide adenine dinucleotide in the mitochondria and reducing reactive oxygen species, it also suppresses lipid peroxidation in rat brain homogenates. This study was to assess the effects of anthraquinone derivatives, rhein on synaptic transmission in the rat hippocampal CA1 pyramidal cell layer by intracellular recording.Methods The excitatory postsynaptic potential (EPSP) evoked by stimulation of the Schaffer collaterals in the presence of bicuculline (15 μmol/L) was depressed by application of rhein (0.3-30 μmol/L). The amplitude of the EPSP was restored within 20 minutes after removal of rhein from the supernatant. At a concentration of 30 μmol/L, rhein reduced the amplitude of the EPSP to 42%±3.7% (n=24) of the control. Subsequently, wavelet spectral entropy was used to analyze the EPSP. Results A strong positive correlation was observed between the wavelet spectral entropy and other parameters such as amplitude, slope of rising phase and slope of descending phase of the EPSP. The paired-pulse facilitation (PPF) of the EPSP was significantly increased by rhein (30 μmol/L). The inhibitory postsynaptic potential (IPSP) recorded in the presence of CNQX (20 μmol/L) and APV (40 μmol/L) is not altered by rhein (30 μmol/L). Conclusions Rhein (30 μmol/L) can decrease the frequency but not the amplitude of the miniature EPSP (mEPSP). It is suggested that rhein inhibits excitatory synaptic transmission by decreasing the release of glutamate in rat hippocampal CA1 pyramidal neurons.

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作者单位: Institute of Biomedical Engineering, Xi'an Jiaotong University, Xi'an 710049, China;Department of Neurosurgery, PLA General Hospital of Chengdu Military Command, Chengdu 610083, China [1] Institute of Biomedical Engineering, Xi'an Jiaotong University, Xi'an 710049, China [2] Department of Physiology, Kurume University School of Medicine, Kurume 830-0011,Japan [3] Department of Physiology, Kurume University School of Medicine, Kurume 830-0011,Japan;Cognitive & Molecular Research Institute of Brain Disease, Open Research Center, Kurume University, 67 Asahi-machi, Kurume 830-0011, Japan [4] Department of Neurosurgery, PLA General Hospital of Chengdu Military Command, Chengdu 610083, China [5]
期刊: 《中华医学杂志(英文版)》2005年118卷10期 817-823页 SCISCIEMEDLINEISTICCSCDCABP
分类号: R3
发布时间: 2005-07-07
基金项目:
国家自然科学基金
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