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一种由基因定义的不对称性是屈肌-伸肌运动性运动抑制控制的基础。

A genetically defined asymmetry underlies the inhibitory control of flexor-extensor locomotor movements.

作者信息

Britz Olivier, Zhang Jingming, Grossmann Katja S, Dyck Jason, Kim Jun C, Dymecki Susan, Gosgnach Simon, Goulding Martyn

机构信息

Molecular Neurobiology Laboratory, Salk Institute for Biological Studies, La Jolla, United States.

Department of Physiology, University of Alberta, Edmonton, Canada.

出版信息

Elife. 2015 Oct 14;4:e04718. doi: 10.7554/eLife.04718.

DOI:10.7554/eLife.04718
PMID:26465208
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4604447/
Abstract

V1 and V2b interneurons (INs) are essential for the production of an alternating flexor-extensor motor output. Using a tripartite genetic system to selectively ablate either V1 or V2b INs in the caudal spinal cord and assess their specific functions in awake behaving animals, we find that V1 and V2b INs function in an opposing manner to control flexor-extensor-driven movements. Ablation of V1 INs results in limb hyperflexion, suggesting that V1 IN-derived inhibition is needed for proper extension movements of the limb. The loss of V2b INs results in hindlimb hyperextension and a delay in the transition from stance phase to swing phase, demonstrating V2b INs are required for the timely initiation and execution of limb flexion movements. Our findings also reveal a bias in the innervation of flexor- and extensor-related motor neurons by V1 and V2b INs that likely contributes to their differential actions on flexion-extension movements.

摘要

V1和V2b中间神经元(INs)对于产生交替的屈肌-伸肌运动输出至关重要。利用一种三联基因系统选择性地消融尾侧脊髓中的V1或V2b中间神经元,并评估它们在清醒行为动物中的特定功能,我们发现V1和V2b中间神经元以相反的方式发挥作用,以控制由屈肌-伸肌驱动的运动。消融V1中间神经元会导致肢体过度屈曲,这表明V1中间神经元衍生的抑制作用对于肢体的正常伸展运动是必需的。V2b中间神经元的缺失会导致后肢过度伸展以及从站立期到摆动期的过渡延迟,这表明V2b中间神经元是肢体屈曲运动及时启动和执行所必需的。我们的研究结果还揭示了V1和V2b中间神经元在与屈肌和伸肌相关的运动神经元支配上存在偏向性,这可能导致它们对屈伸运动产生不同的作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/c52208584957/elife04718fs005.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/c52208584957/elife04718fs005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/4cd0d47b27ae/elife04718f001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/d78342102574/elife04718f002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/651ef9075867/elife04718fs001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/836fe0a174bc/elife04718f003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/913e44b1542c/elife04718f004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/55609052410e/elife04718f005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/3af9e2550da3/elife04718f006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/d7673734d153/elife04718fs002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/20e951ca3252/elife04718fs003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/61a8503695f5/elife04718fs004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/cf42a82e27c6/elife04718f007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/84166bc990a7/elife04718f008.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8686/4604447/c52208584957/elife04718fs005.jpg

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