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黄芪甲苷IV抑制海马神经元的自发突触传递和同步Ca2+振荡。

Astragaloside IV inhibits spontaneous synaptic transmission and synchronized Ca2+ oscillations on hippocampal neurons.

作者信息

Zhu Shao-qing, Qi Lei, Rui Yan-fang, Li Ru-xin, He Xiang-ping, Xie Zuo-ping

机构信息

Department of Biological Science and Biotechnology, State Key Laboratory of Biomembrane and Membrane Biotechnology, Tsinghua University, Beijing, China.

出版信息

Acta Pharmacol Sin. 2008 Jan;29(1):57-64. doi: 10.1111/j.1745-7254.2008.00712.x.

DOI:10.1111/j.1745-7254.2008.00712.x
PMID:18158866
Abstract

AIM

To investigate the changes in the spontaneous neuronal excitability induced by astragaloside IV (AGS-IV) in the cultured hippocampal network.

METHODS

Hippocampal neurons in culture for 9-11 d were used for this study. The spontaneous synaptic activities of these hippocampal neurons were examined by Ca2+ imaging and whole-cell patch-clamp techniques. In total, 40 mg/L AGS-IV dissolved in DMSO and 2 mL/L DMSO were applied to the neurons under a microscope while the experiments were taking place.

RESULTS

AGS-IV inhibited the frequencies of synchronized spontaneous Ca2+ oscillations to 59.39%+/- 3.25%(mean+/-SEM), the spontaneous postsynaptic currents to 43.78%+/- 7.72%(mean+/-SEM), and the spontaneous excitatory postsynaptic currents to 49.25%+/- 7.06%(mean+/-SEM) of those of the control periods, respectively, at 16 min after the AGSIV applications. AGS-IV also decreased the peak values of the voltage-gated K+ and Na+ channel currents at that time point.

CONCLUSION

These results indicate that AGS-IV suppresses the spontaneous neuronal excitabilities effectively. Such a modulation of neuronal activity could represent new evidence for AGS-IV as a neuroprotector.

摘要

目的

研究黄芪甲苷(AGS-IV)对培养的海马神经网络中神经元自发兴奋性的影响。

方法

本研究采用培养9-11天的海马神经元。通过Ca2+成像和全细胞膜片钳技术检测这些海马神经元的自发突触活动。在显微镜下进行实验时,将溶于二甲基亚砜(DMSO)的40mg/L AGS-IV和2mL/L DMSO应用于神经元。

结果

应用AGS-IV 16分钟后,其分别将同步自发Ca2+振荡频率抑制至对照期的59.39%±3.25%(平均值±标准误),将自发突触后电流抑制至43.78%±7.72%(平均值±标准误),将自发兴奋性突触后电流抑制至49.25%±7.06%(平均值±标准误)。此时AGS-IV还降低了电压门控K+和Na+通道电流的峰值。

结论

这些结果表明,AGS-IV能有效抑制神经元的自发兴奋性。这种对神经元活动的调节可能为AGS-IV作为神经保护剂提供新的证据。

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