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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Fos And Jun Potentiate Individual Release Sites And Mobilize The Reserve Synaptic-vesicle Pool At The Drosophila Larval Motor Synapse
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Fos And Jun Potentiate Individual Release Sites And Mobilize The Reserve Synaptic-vesicle Pool At The Drosophila Larval Motor Synapse

机译:Fos和Jun增强果蝇幼虫运动突触的单个释放位点并动员储备突触小泡池。

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摘要

In all nervous systems, short-term enhancement of transmitter release is achieved by increasing the weights of unitary synapses; in contrast, long-term enhancement, which requires nuclear gene expression, is generally thought to be mediated by the addition of new synaptic vesicle release sites. In Drosophila motor neurons, induction of AP-1, a heterodimer of Fos and Jun, induces cAMP- and CREB-dependent forms of presynaptic enhancement. Light and electron microscopic studies indicate that this synaptic enhancement is caused by increasing the weight of unitary synapses and not through the insertion of additional release sites. Electrophys-iological and optical measurements of vesicle dynamics demonstrate that enhanced neurotransmitter release is accompanied by an increase in the actively cycling synaptic vesicle pool at the expense of the reserve pool. Finally, the observation that AP-1 mediated enhancement eliminates tetanus-induced forms of presynaptic potentiation suggests: (i)that reserve-pool mobilization is required for tetanus-induced short-term synaptic plasticity; and (ii) that long-term synaptic plasticity may, in some instances, be accomplished by stable recruitment of mechanisms that normally underlie short-term synaptic change.
机译:在所有神经系统中,通过增加单一突触的权重可以实现短期释放递质。相反,通常认为需要增强核基因表达的长期增强是通过增加新的突触小泡释放位点来介导的。在果蝇运动神经元中,AP-1(Fos和Jun的异二聚体)的诱导诱导cAMP和CREB依赖性的突触前增强形式。光和电子显微镜研究表明,这种突触增强是由于增加单一突触的重量而不是通过插入其他释放位点引起的。囊泡动力学的电生理和光学测量表明,神经递质的释放增加,伴随着主动循环的突触囊泡池的增加,但以储备池为代价。最后,关于AP-1介导的增强作用消除了破伤风诱导的突触前增强作用的观察结果表明:(i)破伤风诱导的短期突触可塑性需要储备池动员; (ii)在某些情况下,可以通过稳定募集通常是短期突触变化基础的机制来实现长期的突触可塑性。

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