Stimulation of the group I extensor afferents prolongs the stance phase in walking cats
Stimulation of the group I extensor afferents prolongs the stance phase in walking cats
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刺激 I 组伸肌传入可延长行走猫的站立期
DOI：
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发表时间：
2004
影响因子：
2
通讯作者：
Keir G. Pearson
中科院分区：
文献类型：
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作者：
Patrick J. Whelan;G. W. Hiebert;Keir G. Pearson
在神经中，I组神经胃胃 - 甲骨髓（LG-SOL），Plantaris（P1）和股外侧/Intermedius（VL/VI）的肌肉在刺激猫中刺激了刺激的刺激。在媒体中爆发的发作之后，用长刺激训练（> 600毫秒）刺激了所有三个神经，从而延长了延长的爆发，并延迟了屈肌爆发活动的发作。 LG-SOL刺激具有强大的效果，直到刺激训练的结束为止增加周期周期所需的最小刺激强度为1.3×阈值，同时刺激P1和VL/VI神经在1.3倍阈值和1.6×阈值之间产生了更大的影响。循环周期比单独刺激任何一个神经。系统通常会在姿势阶段结束时产生异质扩展器EMG的放大器。刺激传入与运动神经元之间的单突触连接，这表明兴奋是通过弱突触的弹性弹药量在300毫秒的弯曲阶段引起的。并重新定位阶段的姿势阶段。 I组的延伸器是要引起这种效应的。由于它们的激活已被证明在减少的脊柱制剂中延长了爆发活性，因此我们的结果支持了后来卸载后肢的假设姿势是步行动物中摆动阶段启动的必要条件。
Group I afferents in nerves innervating the lateral gastrocnemius-soleus (LG-Sol), plantaris (P1), and vastus lateralis/intermedius (VL/VI) muscles were stimulated during walking in decerebrate cats. The stimulus trains were triggered at a fixed delay following the onset of bursts in the medial gastrocnemius muscle. Stimulation of all three nerves with long stimulus trains (>600 ms) prolonged the extensor bursts and delayed the onset of flexor burst activity. LG-Sol nerve stimulation had the strongest effect; often delaying the onset of flexor burst activity until the stimulus train was ended. By contrast, flexor bursts were usually initiated before the end of the stimulus train to the P1 and VL/VI nerves. The minimum stimulus strength required to increase the cycle period was between 1.3×threshold and 1.6×threshold for all three nerves. Simultaneous stimulation of the P1 and VL/VI nerves produced a larger effect on the cycle period than stimulation of either nerve alone. The spatial summation of inputs from knee and ankle muscles suggests that the excitatory action of the group I afferents during the stance phase is distributed to all leg extensor muscles. Stimulation of the group I afferents in extensor nerves generally produced an increase in the amplitude of the heteronymous extensor EMG towards the end of the stance phase. This increase in amplitude occurred even though there were only weak monosynaptic connections between the stimulated afferents and the motoneurones that innervated these heteronymous muscles. This suggests that the excitation was produced via oligosynaptic projections onto the extensor motoneuronal pool. Stimulation with 300 ms trains during the early part of flexion resulted in abrupt termination of the swing phase and reinitiation of the stance phase of the step cycle. The swing phase resumed coincidently with the stimulus offset. Usually, stimulation of two extensor nerves at group I strengths was required to elicit this effect. We were unable to establish the relative contributions of input from the group 1a and group 1b afferents to prolonging the stance phase. However, we consider it likely that group Ib afferents contribute significantly, since their activation has been shown to prolong extensor burst activity in reduced spinal preparations. Thus, our results add support to the hypothesis that unloading of the hindlimb during late stance is a necessary condition for the initiation of the swing phase in walking animals.