Analysis of NPR-1 reveals a circuit mechanism for behavioral quiescence in C. elegans.
Analysis of NPR-1 reveals a circuit mechanism for behavioral quiescence in C. elegans.
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DOI：
10.1016/j.neuron.2013.04.002
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发表时间：
2013-06-05
期刊：
影响因子：
16.2
通讯作者：
Kaplan JM
中科院分区：
文献类型：
--
作者：
Choi S;Chatzigeorgiou M;Taylor KP;Schafer WR;Kaplan JM
动物会因环境、昼夜节律或发育线索而经历行为静止和觉醒的时期。在幼虫蜕皮期间，线虫会经历一段被称为“昏睡”的深刻的行为静止期。在缺乏神经肽受体（NPR-1）的突变体中，昏睡期间的运动静止被消除，并且在缺乏 NPR-1 配体（FLP-18 和 -21）的突变体中减少。野生型菌株的 npr-1 基因具有多态性，它们的昏睡行为也相应变化。运动静止和唤醒是由中枢神经元中唤醒神经肽（PDF-1）分泌的减少和增加介导的。外周机械感觉神经元中表达的 PDF 受体 (PDFR-1) 增强了触摸诱发的钙瞬变。因此，中枢回路通过增强体内外周机械感觉神经元的敏感性来刺激昏睡的唤醒。这些结果定义了一种控制发育编程静止形式的电路机制。
Animals undergo periods of behavioral quiescence and arousal in response to environmental, circadian, or developmental cues. During larval molts, C. elegans undergoes a period of profound behavioral quiescence termed lethargus. Locomotion quiescence during lethargus was abolished in mutants lacking a neuropeptide receptor (NPR-1), and was reduced in mutants lacking NPR-1 ligands (FLP-18 and -21). Wild type strains are polymorphic for the npr-1 gene, and their lethargus behavior varies correspondingly. Locomotion quiescence and arousal were mediated by decreased and increased secretion of an arousal neuropeptide (PDF-1) from central neurons. PDF receptors (PDFR-1) expressed in peripheral mechanosensory neurons enhanced touch-evoked calcium transients. Thus, a central circuit stimulates arousal from lethargus by enhancing the sensitivity of peripheral mechanosensory neurons in the body. These results define a circuit mechanism controlling a developmentally programmed form of quiescence.
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