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(+)-表克拉屈胺,而不是(-)-表克拉屈胺,在促进海马突触 CA1 区的突触传递方面比(-)-克拉屈胺更有潜力。

(+)-epi-Clausenamide, but not (-)-epi-clausenamide, showed more potential than (-)-clausenamide on facilitating synaptic transmission in CA1 region of hippocampal synapses.

机构信息

State Key Laboratory of Bioactive Substances and Functions of Natural Medicines, Institute of Materia Medica, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing, PR China.

出版信息

Neurosci Lett. 2012 Aug 15;523(2):99-103. doi: 10.1016/j.neulet.2012.06.049. Epub 2012 Jun 27.

Abstract

Effect of (+)-epi-clausenamide and (-)-epi-clausenamide on synaptic transmission in CA1 region of hippocampal slice was compared in this study. (+)-epi-Clausenamide showed more potency than (-)-clausenamide on either induction or maintenance of long term potentiation (LTP). Effect of (+)-epi-clausenamide on potentiating basic synaptic transmission was also superior to (-)-clausenamide. However, (-)-epi-clausenamide showed only slight effects on synaptic transmission, suggesting that the effect of (+)-epi-clausenamide and (-)-epi-clausenamide on synaptic transmission depended on their chirality. Calcium influx was not involved in (+)-epi-clausenamide facilitating synaptic transmission in this study. (+)-epi-Clausenamide might promote glutamate release through the activation of Synapsin I(Ser9) to activate the downstream effectors which play a key role in synaptic plasticity. Elucidating the mechanism of each optical isomer of clausenamide by electrophysiological methods provided basis for therapeutic strategies for neurological disorders.

摘要

本研究比较了 (+)-表克劳森酰胺和 (-)-表克劳森酰胺对海马脑片 CA1 区突触传递的影响。(+)表克劳森酰胺在诱导或维持长时程增强(LTP)方面比 (-)-克劳森酰胺更有效。(+)表克劳森酰胺增强基础突触传递的作用也优于 (-)-克劳森酰胺。然而,(-)-表克劳森酰胺对突触传递仅显示出轻微的影响,表明 (+)-表克劳森酰胺和 (-)-表克劳森酰胺对突触传递的影响取决于它们的手性。在本研究中,钙离子内流不参与 (+)-表克劳森酰胺促进突触传递。(+)表克劳森酰胺可能通过激活 Synapsin I(Ser9)促进谷氨酸释放,从而激活在突触可塑性中起关键作用的下游效应物。通过电生理方法阐明克劳森酰胺每个光学异构体的机制为神经紊乱的治疗策略提供了依据。

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