Windhorst U, Christakos C N, Koehler W, Hamm T M, Enoka R M, Stuart D G
Brain Res. 1986 Nov 19;398(1):181-4. doi: 10.1016/0006-8993(86)91266-7.
In anaesthetized cats, medial gastrocnemius motor units (MUs) were electrically stimulated via their ventral-root axons with independent random patterns. Isometric muscle tension and homonymous alpha-motoneuron (MN) membrane-potential fluctuations in response to these stimuli were recorded simultaneously, usually for periods of about 2 min. The tension and membrane potential were averaged with respect to a stimulus train over two disjoint time intervals, one stretching 20-40 s at record beginning, and the other a similar duration at the end of recording. Whereas average MU twitch amplitudes usually decreased between these periods, average membrane potential trajectories did not do so, such that, when normalized to the change in twitch amplitude, the membrane potential trajectories usually increased in size. This suggests that the decline in the mechanical effect of MU activation was accompanied by an increase in the gain of the afferent pathway to homonymous MNs, which was confirmed by gain computations in the frequency domain. This compensation could be a mechanism to maintain the high quality of information about MU contractions transmitted to MNs in the course of MU fatigue.
在麻醉猫中，通过其腹根轴突以独立随机模式对腓肠肌内侧运动单位（MU）进行电刺激。同时记录等长肌肉张力和同体α运动神经元（MN）对这些刺激的膜电位波动，通常记录约2分钟。在两个不相交的时间间隔内，将张力和膜电位相对于刺激序列进行平均，一个在记录开始时延伸20 - 40秒，另一个在记录结束时持续类似时长。虽然平均MU抽搐幅度通常在这些时间段之间下降，但平均膜电位轨迹并非如此，因此，当根据抽搐幅度的变化进行归一化时，膜电位轨迹通常会增大。这表明MU激活的机械效应下降伴随着传入同体MN通路增益的增加，这在频域中的增益计算中得到了证实。这种补偿可能是一种机制，用于在MU疲劳过程中维持传递给MN的关于MU收缩的高质量信息。
