Kim Hojeong
Convergence Research Institute, Daegu Gyeongbuk Institute of Science and Technology, Daegu, South Korea
J Appl Physiol (1985). 2017 Jul 1;123(1):88-105. doi: 10.1152/japplphysiol.00491.2016. Epub 2017 Mar 23.
Persistent inward current (PIC)-generating Ca1.3 channels in spinal motoneuron dendrites are thought to be actively recruited during normal behaviors. However, whether and how the activation of PIC channels influences force output of motor unit remains elusive. Here, building a physiologically realistic model of slow motor unit I demonstrated that force production induced by the PIC activation is much smaller for short than lengthened muscles during the regular firing of the motoneuron that transitions from the quiescent state by either a brief current pulse at the soma or a brief synaptic excitation at the dendrites. By contrast, the PIC-induced force potentiation was maximal for short muscles when the motoneuron switched from a stable low-frequency firing state to a stable high-frequency firing state by the current pulse at the soma. Under the synaptic excitation at the dendrites, however, the force could not be potentiated by the transitioning of the motoneuron from a low- to a high-frequency firing state due to the simultaneous onset of PIC at the dendrites and firing at the soma. The strong dependency of the input-output relationship of the motor unit on the neuromodulation and Ia afferent inputs for the PIC channels was further shown under static variations in muscle length. Taken together, these findings suggest that the PIC activation in the motoneuron dendrites may differentially affect the force production of the motor unit, depending not only on the firing state history of the motoneuron and the variation in muscle length but also on the mode of motor activity. Ca1.3 channels in motoneuron dendrites are actively involved during normal motor activities. To investigate the effects of the activation of motoneuron Ca1.3 channels on force production, a model motor unit was built based on best-available data. The simulation results suggest that force potentiation induced by Ca1.3 channel activation is strongly modulated not only by firing history of the motoneuron but also by length variation of the muscle as well as neuromodulation inputs from the brainstem.
脊髓运动神经元树突中产生持续性内向电流（PIC）的Ca1.3通道被认为在正常行为中会被积极募集。然而，PIC通道的激活是否以及如何影响运动单位的力输出仍然不清楚。在此，通过构建一个生理现实的慢运动单位模型，我证明了在运动神经元从静息状态通过胞体的短暂电流脉冲或树突的短暂突触兴奋转变为正常放电时，PIC激活诱导的力产生在短肌肉中比在拉长肌肉中要小得多。相比之下，当运动神经元通过胞体的电流脉冲从稳定的低频放电状态转变为稳定的高频放电状态时，PIC诱导的力增强在短肌肉中最大。然而，在树突的突触兴奋下，由于树突处PIC的同时发生和胞体的放电，运动神经元从低频放电状态转变为高频放电状态时，力无法增强。在肌肉长度的静态变化下，进一步显示了运动单位的输入-输出关系对PIC通道的神经调节和Ia传入输入的强烈依赖性。综上所述，这些发现表明，运动神经元树突中的PIC激活可能会对运动单位的力产生产生不同的影响，这不仅取决于运动神经元的放电状态历史和肌肉长度的变化，还取决于运动活动的模式。运动神经元树突中的Ca1.3通道在正常运动活动中积极参与。为了研究运动神经元Ca1.3通道激活对力产生的影响，基于现有最佳数据构建了一个模型运动单位。模拟结果表明，Ca1.3通道激活诱导 的力增强不仅受到运动神经元放电历史的强烈调节，还受到肌肉长度变化以及来自脑干的神经调节输入的强烈调节。
