Role of tyramine in calcium dynamics of GABAergic neurons and escape behavior in Caenorhabditis elegans.
Role of tyramine in calcium dynamics of GABAergic neurons and escape behavior in Caenorhabditis elegans.
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DOI：
10.1186/s40851-018-0103-1
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发表时间：
2018
影响因子：
2.7
通讯作者：
Nakai J
中科院分区：
文献类型：
--
作者：
Kagawa-Nagamura Y;Gengyo-Ando K;Ohkura M;Nakai J
酪胺在哺乳动物中被称为“微量胺”，调节无脊椎动物的广泛行为;然而，其潜在的细胞和电路机制尚不清楚。秀丽隐杆线虫（C.然而，酪胺影响关键行为，包括觅食、进食和逃避反应。触摸诱发的向后逃避反应通常伴随着一个急剧的欧米茄转向，使动物能够向相反的方向航行。先前的研究表明，GABA能体运动神经元中的代谢型酪胺受体SER-2控制欧米茄转弯中的身体深部弯曲。本研究主要探讨酪胺在GABA能头部运动神经元中的作用。我们的目标是了解酪胺能信号改变神经回路活动以控制逃避行为的机制。在自由运动的C.在elegans中，我们发现头部中的GABA能RME运动神经元在向前运动期间具有高钙水平，但在自发和诱发的向后运动期间具有低钙水平。这种钙的减少也观察到在欧米茄转。突变体分析表明，tbh-1突变体缺乏章鱼胺有正常的钙反应，而TDC-1突变体缺乏酪胺和章鱼胺并没有表现出RME钙减少。这种神经调节由SER-2介导。此外，酪胺能RIM神经元的活性与RME活性呈负相关的方向开关从向前到向后运动。这些结果表明从RIM释放的酪胺通过SER-2信号传导抑制RME。当动物重新开始向前运动时，通过头部的急剧弯曲来启动欧米茄转向。有趣的是，ser-2突变体表现出浅的头部弯曲，并且经常无法执行深角度的欧米茄转弯。在RME中表达SER-2可以挽救SER-2突变体的行为缺陷和异常的钙反应。这些结果表明，酪胺能抑制RME参与控制的欧米茄转向。我们证明，内源性酪胺下调钙水平GABA能RME运动神经元在头部通过酪胺受体SER-2在向后运动和欧米茄转动。我们的数据表明，这种神经调节允许在欧米茄转动时头部深弯曲，并在C.优美的本文的在线版本（10.1186/s40851-018-0103-1）包含补充材料，可供授权用户使用。
Tyramine, known as a “trace amine” in mammals, modulates a wide range of behavior in invertebrates; however, the underlying cellular and circuit mechanisms are not well understood. In the nematode Caenorhabditis elegans (C. elegans), tyramine affects key behaviors, including foraging, feeding, and escape responses. The touch-evoked backward escape response is often coupled with a sharp omega turn that allows the animal to navigate away in the opposite direction. Previous studies have showed that a metabotropic tyramine receptor, SER-2, in GABAergic body motor neurons controls deep body bending in omega turns. In this study, we focused on the role of tyramine in GABAergic head motor neurons. Our goal is to understand the mechanism by which tyraminergic signaling alters neural circuit activity to control escape behavior. Using calcium imaging in freely moving C. elegans, we found that GABAergic RME motor neurons in the head had high calcium levels during forward locomotion but low calcium levels during spontaneous and evoked backward locomotion. This calcium decrease was also observed during the omega turn. Mutant analyses showed that tbh-1 mutants lacking only octopamine had normal calcium responses, whereas tdc-1 mutants lacking both tyramine and octopamine did not exhibit the calcium decrease in RME. This neuromodulation was mediated by SER-2. Moreover, tyraminergic RIM neuron activity was negatively correlated with RME activity in the directional switch from forward to backward locomotion. These results indicate that tyramine released from RIM inhibits RME via SER-2 signaling. The omega turn is initiated by a sharp head bend when the animal reinitiates forward movement. Interestingly, ser-2 mutants exhibited shallow head bends and often failed to execute deep-angle omega turns. The behavioral defect and the abnormal calcium response in ser-2 mutants could be rescued by SER-2 expression in RME. These results suggest that tyraminergic inhibition of RME is involved in the control of omega turns. We demonstrate that endogenous tyramine downregulates calcium levels in GABAergic RME motor neurons in the head via the tyramine receptor SER-2 during backward locomotion and omega turns. Our data suggest that this neuromodulation allows deep head bending during omega turns and plays a role in the escape behavior in C. elegans. The online version of this article (10.1186/s40851-018-0103-1) contains supplementary material, which is available to authorized users.
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影响因子：
9.8
作者：
Donnelly JL;Clark CM;Leifer AM;Pirri JK;Haburcak M;Francis MM;Samuel AD;Alkema MJ
通讯作者：
Alkema MJ
影响因子：
48
作者：
Guo, Zengcai V.;Hart, Anne C.;Ramanathan, Sharad
通讯作者：
Ramanathan, Sharad
影响因子：
2.5
作者：
Bacon, JP;Thompson, KSJ;Stern, M
通讯作者：
Stern, M
影响因子：
64.8
作者：
Bendesky, Andres;Tsunozaki, Makoto;Rockman, Matthew V.;Kruglyak, Leonid;Bargmann, Cornelia I.
通讯作者：
Bargmann, Cornelia I.
DOI：
10.1073/pnas.0409009101
发表时间：
2005-03-01
影响因子：
11.1
作者：
Gray, JM;Hill, JJ;Bargmann, CI
通讯作者：
Bargmann, CI