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B 型运动神经元的过度激活导致秀丽隐杆线虫运动回路的异常同步。

Hyperactivation of B-type motor neurons results in aberrant synchrony of the Caenorhabditis elegans motor circuit.

机构信息

Institute of Developmental and Regenerative Biology, School of Life and Environmental Sciences, Hangzhou Normal University, 310036 Hangzhou, China.

出版信息

J Neurosci. 2013 Mar 20;33(12):5319-25. doi: 10.1523/JNEUROSCI.4017-12.2013.

Abstract

Excitatory acetylcholine motor neurons drive Caenorhabditis elegans locomotion. Coordinating the activation states of the backward-driving A and forward-driving B class motor neurons is critical for generating sinusoidal and directional locomotion. Here, we show by in vivo calcium imaging that expression of a hyperactive, somatodendritic ionotropic acetylcholine receptor ACR-2(gf) in A and B class motor neurons induces aberrant synchronous activity in both ventral- and dorsal-innervating B and A class motor neurons. Expression of ACR-2(gf) in either ventral- or dorsal-innervating B neurons is sufficient for triggering the aberrant synchrony that results in arrhythmic convulsions. Silencing of AVB, the premotor interneurons that innervate B motor neurons suppresses ACR-2(gf)-dependent convulsion; activating AVB by channelrhodopsin induces the onset of convulsion. These results support that the activity state of B motor neurons plays an instructive role for the coordination of motor circuit.

摘要

兴奋性乙酰胆碱运动神经元驱动秀丽隐杆线虫的运动。协调向后驱动的 A 类和向前驱动的 B 类运动神经元的激活状态对于产生正弦和定向运动至关重要。在这里,我们通过体内钙成像表明,在 A 和 B 类运动神经元中表达超活性的躯体树突型离子型乙酰胆碱受体 ACR-2(gf)会诱导腹侧和背侧支配的 B 和 A 类运动神经元的异常同步活动。在腹侧或背侧支配的 B 神经元中表达 ACR-2(gf)足以引发导致节律性抽搐的异常同步。沉默支配 B 运动神经元的中间神经元 AVB 可抑制 ACR-2(gf)依赖性抽搐;通过通道视紫红质激活 AVB 会引起抽搐发作。这些结果表明 B 运动神经元的活动状态对于运动回路的协调起着指导作用。

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