Neuronal plasticity regulated by the insulin-like signaling pathway underlies salt chemotaxis learning in Caenorhabditis elegans
Neuronal plasticity regulated by the insulin-like signaling pathway underlies salt chemotaxis learning in Caenorhabditis elegans
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DOI：
10.1152/jn.01029.2010
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发表时间：
2011-07-01
影响因子：
2.5
通讯作者：
Iino, Yuichi
中科院分区：
文献类型：
--
作者：
Oda, Shigekazu;Tomioka, Masahiro;Iino, Yuichi
S，Tomioka M，Iino Y。胰岛素样信号通路调节的神经元可塑性是秀丽线虫学习盐趋化的基础。神经生理学杂志106：301-308,2011。2011年4月27日首次出版；DOI：10.1152/jn.01029.2010。-量化活动物的神经元可塑性对于理解学习和记忆是必不可少的。秀丽线虫对氯化钠表现出趋化行为。然而，在饥饿条件下长期暴露在氯化钠中后，它学会了避免氯化钠，这被称为盐趋化性学习。胰岛素样信号对盐敏感觉神经元ASER的这种行为可塑性和功能具有重要作用。然而，包括ASER在内的神经元如何显示神经元可塑性尚不清楚。为了确定与盐趋化学习相关的神经元可塑性，我们用活体成像技术测量了单个神经元的钙反应和突触释放。我们发现，在没有食物的情况下，长时间暴露于NaC l后，ASER的反应增强，而其突触释放减少。这些相反方向的变化在胰岛素样信号突变体中被取消，表明胰岛素样信号调节ASER中的这些可塑性。下游中间神经元之一AIB的反应在氯化钠处理后显著降低。AIB反应的这种改变不依赖于胰岛素样信号通路。我们的结果表明，在盐趋化学习中，有关盐的信息在感觉神经元和中间神经元的水平上都受到调制。
Oda S, Tomioka M, Iino Y. Neuronal plasticity regulated by the insulin-like signaling pathway underlies salt chemotaxis learning in Caenorhabditis elegans. J Neurophysiol 106: 301-308, 2011. First published April 27, 2011; doi:10.1152/jn.01029.2010.-Quantification of neuronal plasticity in a living animal is essential for understanding learning and memory. Caenorhabditis elegans shows a chemotactic behavior toward NaCl. However, it learns to avoid NaCl after prolonged exposure to NaCl under starvation conditions, which is called salt chemotaxis learning. Insulin-like signaling is important for this behavioral plasticity and functions in one of the salt-sensing sensory neurons, ASE right (ASER). However, how neurons including ASER show neuronal plasticity is unknown. To determine the neuronal plasticity related to salt chemotaxis learning, we measured Ca(2+) response and synaptic release of individual neurons by using in vivo imaging techniques. We found that response of ASER increased whereas its synaptic release decreased after prolonged exposure to NaCl without food. These changes in the opposite directions were abolished in insulin-like signaling mutants, suggesting that insulin-like signaling regulates these plasticities in ASER. The response of one of the downstream interneurons, AIB, decreased profoundly after NaCl conditioning. This alteration in AIB response was independent of the insulin-like signaling pathway. Our results suggest that information on NaCl is modulated at the level of both sensory neurons and interneurons in salt chemotaxis learning.