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首页> 外文期刊>Neuron >A neuropeptide-mediated stretch response links muscle contraction to changes in neurotransmitter release.
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A neuropeptide-mediated stretch response links muscle contraction to changes in neurotransmitter release.

机译:神经肽介导的拉伸反应将肌肉收缩与神经递质释放的变化联系起来。

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Although Caenorhabditis elegans has been utilized extensively to study synapse formation and function, relatively little is known about synaptic plasticity in C. elegans. We show that a brief treatment with the cholinesterase inhibitor aldicarb induces a form of presynaptic potentiation whereby ACh release at neuromuscular junctions (NMJs) is doubled. Aldicarb-induced potentiation was eliminated by mutations that block processing of proneuropeptides, by mutations inactivating a single proneuropeptide (NLP-12), and by those inactivating an NLP-12 receptor (CKR-2). NLP-12 expression is limited to a single stretch-activated neuron, DVA. Analysis of a YFP-tagged NLP-12 suggests that aldicarb stimulates DVA secretion of NLP-12. Mutations disrupting the DVA mechanoreceptor (TRP-4) decreased aldicarb-induced NLP-12 secretion and blocked aldicarb-induced synaptic potentiation. Mutants lacking NLP-12 or CKR-2 have decreased locomotion rates. Collectively, these results suggest that NLP-12 mediates a mechanosensory feedback loop that couples muscle contraction to changes in presynaptic release, thereby providing a mechanism for proprioceptive control of locomotion.
机译:尽管秀丽隐杆线虫已被广泛用于研究突触的形成和功能,但对秀丽隐杆线虫的突触可塑性了解相对较少。我们显示,胆碱酯酶抑制剂涕灭威的简短治疗诱导突触前增强的一种形式,从而使神经肌肉接头(NMJs)乙酰胆碱释放增加一倍。涕灭威诱导的增强作用可通过阻断前神经肽的加工的突变,使单个前神经肽(NLP-12)失活的突变以及使NLP-12受体(CKR-2)失活的突变而消除。 NLP-12表达仅限于单个拉伸激活的神经元DVA。对带有YFP标签的NLP-12的分析表明涕灭威刺激了NVA-12的DVA分泌。破坏DVA机械感受器(TRP-4)的突变降低了涕灭威诱导的NLP-12分泌并阻断了涕灭威诱导的突触增强。缺少NLP-12或CKR-2的突变体的运动速度降低。总体而言,这些结果表明,NLP-12介导了一个机械感官反馈回路,该回路将肌肉收缩与突触前释放的变化耦合,从而提供了对运动的本体感受控制的机制。

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