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佛波酯增强甲壳类动物神经肌肉接头处的突触传递。

Phorbol ester enhances synaptic transmission at crustacean neuromuscular junctions.

作者信息

Gilat E, Hochner B

机构信息

Otto Loewi Center for Cellular and Molecular Neurobiology, Department of Neurobiology, Hebrew University of Jerusalem, Israel.

出版信息

Synapse. 1990;6(1):91-100. doi: 10.1002/syn.890060111.

DOI:10.1002/syn.890060111
PMID:2169073
Abstract

Effects of phorbol ester (PE) (4 beta-phorbol-12,13-dibutyrate) on transmitter release were studied in the deep extensor neuromuscular system of the prawn, Macrobrachium rosenbergii. Our findings show that PE enhances transmitter release as indicated by an increase in the quantal content. PE had no post-synaptic effects. The increase in release is accompanied by a slight decline in twin pulse facilitation, suggesting a minor increase in Ca2+ entry. The fact that the increase in Ca2+ entry has a minor contribution to the PE effect is supported by the following observations: the duration of facilitation was not affected by PE, and 3,4-diaminopyridine (3,4-DAP), which by itself increased release, did not reduce the effect of PE. The time course of release was measured from synaptic delay histograms, upon which PE had no effect. This finding indicates that protein kinase C (PKC) is probably not involved in the rate limiting step of the process of secretion. The log/log plot of the initial part of the delay histogram is not affected by PE, suggesting a lack of effect on cooperativity of the release process. Increased release by loading the presynaptic terminal with Ca2+ either by pretreatment with Ca2+ ionophore or by frequent stimulation prevented further increase in release by PE. We conclude that the main effect of PE is confined to stages of release that are secondary to the first elevation in presynaptic Ca2+. PKC in this system probably plays a role in long term modulation of release, and it can be activated in processes leading to presynaptic Ca2+ accumulation.

摘要

在罗氏沼虾的深层伸肌神经肌肉系统中,研究了佛波酯(PE)(4β-佛波醇-12,13-二丁酸酯)对递质释放的影响。我们的研究结果表明,如量子含量增加所示,PE增强了递质释放。PE没有突触后效应。释放的增加伴随着双脉冲易化的轻微下降,表明Ca2+内流略有增加。以下观察结果支持Ca2+内流增加对PE效应贡献较小这一事实:易化持续时间不受PE影响,而本身能增加释放的3,4-二氨基吡啶(3,4-DAP)并没有降低PE的效应。从突触延迟直方图测量释放的时间进程,PE对此没有影响。这一发现表明蛋白激酶C(PKC)可能不参与分泌过程的限速步骤。延迟直方图初始部分的对数/对数图不受PE影响,表明对释放过程的协同性没有影响。通过用Ca2+离子载体预处理或频繁刺激使突触前终末负载Ca2+来增加释放,可阻止PE进一步增加释放。我们得出结论,PE的主要作用局限于突触前Ca2+首次升高之后的释放阶段。该系统中的PKC可能在释放的长期调节中起作用,并且它可以在导致突触前Ca2+积累的过程中被激活。

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引用本文的文献

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Mechanisms in the regulation of neurotransmitter release from brain nerve terminals: current hypotheses.调节脑神经末梢神经递质释放的机制:当前假说
Neurochem Res. 1993 Jan;18(1):47-58. doi: 10.1007/BF00966922.