Epidural spinal cord stimulation plus quipazine administration enable stepping in complete spinal adult rats
Epidural spinal cord stimulation plus quipazine administration enable stepping in complete spinal adult rats
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DOI：
10.1152/jn.00836.2007
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发表时间：
2007-11-01
影响因子：
2.5
通讯作者：
Edgerton, V. Reggie
中科院分区：
文献类型：
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作者：
Gerasimenko, Yury P.;Ichiyama, Ronaldo M.;Edgerton, V. Reggie
我们假设硬膜外脊髓刺激（ES）和喹吡嗪（一种血清素能激动剂）以性质独特但互补的方式调节与屈肌和伸肌相关的脊髓内神经网络的兴奋性，从而促进脊髓损伤大鼠的运动。为了验证这一假设，我们在经过双足步行训练和未训练的成年完全性脊髓（胸中部）大鼠中，在腹腔注射喹吡嗪（0.3 mg/kg）前后对S - 1脊髓节段进行（40 Hz）刺激。将这些大鼠的步行模式与对照大鼠进行比较。在所使用的刺激水平下，只有当后肢放在移动的跑步机上时才会引发步行。在未训练的大鼠中，由ES和喹吡嗪给药诱导的步行是不负重的，且周期比对照组短。相比之下，在经过步行训练的大鼠中，由ES和喹吡嗪诱导的步行高度协调，有明显的足底着地和部分负重。ES和喹吡嗪对肌电图爆发幅度和持续时间的影响在屈肌运动群中比在伸肌运动群中更大。通过对ES期间肌电图爆发进行快速傅里叶变换分析，我们观察到内侧腓肠肌（踝关节伸肌）在40 Hz处有一个主峰，而在胫骨前肌（踝关节屈肌）中则较少有主导频谱峰。我们认为这些频率分布反映了伸肌中主要为单突触电位的幅度调制以及屈肌中主要为多突触通路的幅度调制。喹吡嗪增强了这些反应的幅度。数据表明，在运动过程中产生屈肌和伸肌活动的回路存在根本差异。
We hypothesized that epidural spinal cord stimulation (ES) and quipazine (a serotonergic agonist) modulates the excitability of flexor and extensor related intraspinal neural networks in qualitatively unique, but complementary, ways to facilitate locomotion in spinal cord-injured rats. To test this hypothesis, we stimulated (40 Hz) the S-1 spinal segment before and after quipazine administration (0.3 mg/kg, ip) in bipedally step-trained and nontrained, adult, complete spinal (mid-thoracic) rats. The stepping pattern of these rats was compared with control rats. At the stimulation levels used, stepping was elicited only when the hindlimbs were placed on a moving treadmill. In nontrained rats, the stepping induced by ES and quipazine administration was non-weight bearing, and the cycle period was shorter than in controls. In contrast, the stepping induced by ES and quipazine in step-trained rats was highly coordinated with clear plantar foot placement and partial weight bearing. The effect of ES and quipazine on EMG burst amplitude and duration was greater in flexor than extensor motor pools. Using fast Fourier transformation analysis of EMG bursts during ES, we observed one dominant peak at 40 Hz in the medial gastrocnemius (ankle extensor), whereas there was less of dominant spectral peak in the tibialis anterior (ankle flexor). We suggest that these frequency distributions reflect amplitude modulation of predominantly monosynaptic potentials in the extensor and predominantly polysynaptic pathways in the flexor muscle. Quipazine potentiated the amplitude of these responses. The data suggest that there are fundamental differences in the circuitry that generates flexion and extension during locomotion.