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首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Synaptic neuropeptide release induced by octopamine without Ca~(2+) entry into the nerve terminal
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Synaptic neuropeptide release induced by octopamine without Ca~(2+) entry into the nerve terminal

机译：章鱼胺诱导的突触神经肽释放，而Ca〜（2+）不会进入神经末梢

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摘要

Synaptic release of neurotransmitters is evoked by activity-dependent Ca~(2+) entry into the nerve terminal. However, here it is shown that robust synaptic neuropeptide release from Drosophila motoneu-rons is evoked in the absence of extracellular Ca~(2+) by octopamine, the arthropod homolog to norepinephrine. Genetic and pharmacology experiments demonstrate that this surprising peptidergic transmission requires cAMP-dependent protein kinase, with only a minor contribution of exchange protein activated by cAMP (epac). Octop-amine-evoked neuropeptide release also requires endoplasmic re-ticulum Ca~(2+) mobilization by the ryanodine receptor and the inositol trisphosphate receptor. Hence, rather than relying exclusively on activity-dependent Ca~(2+) entry into the nerve terminal, a behavior-ally important neuromodulator uses synergistic cAMP-dependent protein kinase and endoplasmic reticulum Ca~(2+) signaling to induce synaptic neuropeptide release.
机译：依赖于活性的Ca〜（2+）进入神经末梢引起神经递质的突触释放。然而，在此表明，在缺乏胞外Ca〜（2+）的情况下，章鱼胺（去甲肾上腺素的节肢动物同源物）引起了果蝇运动神经元强烈的突触神经肽释放。遗传和药理学实验表明，这种令人惊讶的肽能传递需要cAMP依赖的蛋白激酶，而cAMP（epac）激活的交换蛋白的贡献很小。章鱼胺诱发的神经肽释放也需要内质网Ca〜（2+）通过ryanodine受体和肌醇三磷酸受体动员。因此，行为上重要的神经调节剂不是仅依赖于活动依赖的Ca〜（2+）进入神经末梢，而是使用协同的cAMP依赖蛋白激酶和内质网Ca〜（2+）信号来诱导突触神经肽释放。 。

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