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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Prolonged presynaptic posttetanic cyclic GMP signaling in Drosophila motoneurons
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Prolonged presynaptic posttetanic cyclic GMP signaling in Drosophila motoneurons

机译：果蝇运动神经元中突触前后强直循环GMP信号延长。

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摘要

Ca~(2+) can stimulate cyclic nucleotide synthesis, but it is not known whether this signaling occurs in nerve terminals in response to activity. Here, in vivo imaging of Drosophila motoneuron terminals shows that activity rapidly induces a long-lasting signal from a transgenically expressed optical indicator based on the epac1 (exchange protein directly activated by cAMP 1) cAMP-binding domain. The epac1-cAMP sensor (camps) response in synaptic boutons depends on extracellular Ca~(2+) and ryanodine receptor-mediated Ca~(2+)-induced Ca~(2+) release from the endoplasmic retic-ulum. However, mutations that inhibit rutabaga Ca~(2+)-stimulated adenylyl cyclase and dunce cAMP-specific phosphodiesterase (PDE) have no effect. Instead, the activity-dependent presynaptic epaci-camps signal reflects elevation of cGMP in response to nitric oxide-activated guanylyl cyclase. Posttetanic presynaptic cGMP is long-lived because of limited PDE activity. Thus, nerve terminal biochemical signaling induced by brief bouts of activity temporally summates on a time scale orders of magnitude longer than fast transmission.
机译：Ca〜（2+）可以刺激环状核苷酸的合成，但是尚不清楚该信号是否在神经末梢响应活动而发生。在这里，果蝇运动神经元终端的体内成像显示，该活性迅速诱导了基于epac1（由cAMP 1直接激活的交换蛋白）cAMP结合域的转基因表达光学指示剂产生的持久信号。 epac1-cAMP传感器（营地）在突触钮扣中的反应取决于胞内Ca〜（2+）和ryanodine受体介导的Ca〜（2+）诱导的Ca〜（2+）从内质网释放。但是，抑制大头菜Ca〜（2+）刺激的腺苷酸环化酶和cAMP特异性磷酸二酯酶（PDE）抑制的突变无效。取而代之的是，依赖于活性的突触前间隔信号反映了一氧化氮激活的鸟苷酸环化酶响应时cGMP的升高。由于PDE活性有限，突触后cGMP寿命长。因此，由短暂活动引起的神经末梢生化信号在时间上的累积时间比快速传播长几个数量级。

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