分析 NPR-1 揭示了线虫行为静止的电路机制。
Analysis of NPR-1 reveals a circuit mechanism for behavioral quiescence in C. elegans.
机构信息
Department of Molecular Biology, Massachusetts General Hospital, Boston, MA 02114, USA.
出版信息
Neuron. 2013 Jun 5;78(5):869-80. doi: 10.1016/j.neuron.2013.04.002.
Abstract
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 FLP-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.
摘要
动物会根据环境、昼夜节律或发育线索经历行为静止和觉醒的时期。在幼虫蜕皮期间，秀丽隐杆线虫会经历一段称为昏睡的深度行为静止期。缺乏神经肽受体（NPR-1）的突变体中，昏睡期间的运动静止状态被消除，缺乏 NPR-1 配体（FLP-18 和 FLP-21）的突变体中，这种状态减少。野生型菌株的 npr-1 基因多态性，其昏睡行为也相应变化。运动静止和觉醒是由中枢神经元中觉醒神经肽（PDF-1）的分泌减少和增加介导的。在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，中枢回路通过增强身体外周机械感觉神经元的敏感性来刺激从昏睡中觉醒。这些结果定义了一个控制发育编程形式的静止的电路机制。
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