Heitler W J
The Gatty Marine Laboratory, University of St Andrews, Fife, UK.
Eur J Neurosci. 1995 May 1;7(5):981-92. doi: 10.1111/j.1460-9568.1995.tb01086.x.
The jump and kick of the grasshopper are behaviours which are potentially critical for the survival of the animal, and whose maximal performance depends upon optimizing the rate and level of tension development in the extensor tibiae muscle of the hind legs. In experimental conditions extensor tension control can be reduced to a single motoneuron, the fast extensor tibiae (FETi). The axon of FETi can be cut using dye-mediated laser photoaxotomy without damaging the central or peripheral portions of that neuron or any other neuron innervating the leg. The axotomy can be functionally reversed (i.e. the cut axon repaired) by an electronic axonal bypass which detects FETi spikes on the proximal side of the cut and stimulates the axon on the distal side of the cut. In this way motor spikes can either be allowed to reach the muscle or prevented from doing so (by switching the bypass on or off), and the motor programmes produced with and without extensor tension can be compared. The jump and kick are normally produced by a three-stage motor programme: (i) initial flexion brings the tibia into the fully flexed position; (ii) coactivation of extensor and flexor muscles allows the extensor muscle to develop maximal tension almost isometrically, while the simultaneous contraction of the flexor muscle holds the tibia flexed; (iii) sudden trigger inhibition of the flexor system (motoneurons and muscle) releases the tibia and allows the behaviour to be expressed. The grasshopper can produce fictive kicks with motor programmes which show each of these three major structural features of a normal kick, but without any extensor tension whatsoever. There is no significant difference in the frequency of FETi spikes, the duration of coactivation or the maximum depolarization of the flexor motoneurons between fictive and quasi-normal (i.e. reversed axotomy) kicks. The trigger inhibition of flexor motoneurons is shallower in fictive than in quasi-normal kicks. The significance of this is discussed in relation to the activity of the interneuron M, which is known to mediate trigger inhibition onto FITi motoneurons. There are two main conclusions from this study. First, the CNS does not need feedback from ETi muscle tension in order to produce the three-stage motor programme of the kick (and, by implication, the jump). Second, the CNS does not adjust the frequency or duration of FETi activity in response to unexpected changes in ETi tension. ETi tension appears to be under open-loop control in the kick motor programme.
蚱蜢的跳跃和踢腿行为对其生存可能至关重要，其最佳表现取决于优化后腿胫节伸肌的张力发展速率和水平。在实验条件下，伸肌张力控制可简化为单个运动神经元，即快速胫节伸肌（FETi）。可以使用染料介导的激光光轴切断术切断FETi的轴突，而不会损坏该神经元的中枢或外周部分，也不会损坏支配腿部的任何其他神经元。轴突切断术可通过电子轴突旁路在功能上逆转（即切断的轴突修复），该旁路检测切断近端的FETi尖峰并刺激切断远端的轴突。通过这种方式，运动尖峰既可以到达肌肉，也可以被阻止到达肌肉（通过打开或关闭旁路），并且可以比较有和没有伸肌张力时产生的运动程序。跳跃和踢腿通常由一个三阶段运动程序产生：（i）初始屈曲将胫节带入完全屈曲位置；（ii）伸肌和屈肌的共同激活使伸肌几乎等长地产生最大张力，而屈肌的同时收缩使胫节保持屈曲；（iii）突然触发抑制屈肌系统（运动神经元和肌肉）释放胫节并使行为得以表现。蚱蜢可以通过运动程序产生虚构的踢腿动作，这些程序显示了正常踢腿的这三个主要结构特征，但没有任何伸肌张力。在虚构踢腿和准正常（即轴突切断术逆转）踢腿之间，FETi尖峰的频率、共同激活的持续时间或屈肌运动神经元的最大去极化没有显著差异。虚构踢腿中屈肌运动神经元的触发抑制比准正常踢腿中更浅。这一点的意义将结合中间神经元M的活动进行讨论，已知中间神经元M介导对FITi运动神经元的触发抑制。这项研究有两个主要结论。第一，中枢神经系统在产生踢腿（以及由此推断的跳跃）的三阶段运动程序时不需要来自ETi肌肉张力的反馈。第二，中枢神经系统不会响应ETi张力的意外变化而调整FETi活动的频率或持续时间。在踢腿运动程序中，ETi张力似乎处于开环控制之下。
