Côté Marie-Pascale, Ménard Ariane, Gossard Jean-Pierre
Centre de Recherche en Sciences Neurologiques, Département de Physiologie, Faculté de Médecine, Université de Montréal, Montréal, Québec, Canada H3C 3J7.
J Neurosci. 2003 Apr 1;23(7):2789-96. doi: 10.1523/JNEUROSCI.23-07-02789.2003.
Treadmill training and clonidine, an alpha-2 noradrenergic agonist, have been shown to improve locomotion after spinal cord injury. We speculate that transmission in load pathways, which are involved in body support during stance, is specifically modified by training. This was evaluated by comparing two groups of spinal cats; one group (n = 11) was trained to walk until full-weight-bearing (3-4 weeks), and the other (shams; n = 7) was not. During an acute experiment, changes in group I pathways, monosynaptic excitation, disynaptic inhibition, and polysynaptic excitation were investigated by measuring the response amplitude in extensor motoneurons before and after clonidine injection. Monosynaptic excitation was not modified by clonidine but was decreased significantly by training. Disynaptic inhibition was significantly decreased by clonidine in both groups, but more significantly in trained cats, and significantly reduced by training after clonidine. Also, clonidine could reverse group IB inhibition into polysynaptic excitation in both groups but more frequently in trained cats. We also investigated whether fictive stepping revealed additional changes. In trained cats, the phase-dependent modulation of all three responses was similar to patterns reported previously, but in shams, modulation of monosynaptic and polysynaptic responses was not. Overall, training appears to decrease monosynaptic excitation and enhance the effects of clonidine in the reduction of disynaptic inhibition and reversal to polysynaptic excitation. Because it is believed that polysynaptic excitatory group I pathways transmit locomotor drive to extensor motoneurons, we suggest that the latter changes would facilitate the recruitment of extensor muscles for recovering weight-bearing during stepping.
跑步机训练和可乐定（一种α-2去甲肾上腺素能激动剂）已被证明可改善脊髓损伤后的运动能力。我们推测，在站立时参与身体支撑的负荷通路中的传导会因训练而发生特异性改变。通过比较两组脊髓猫对此进行了评估；一组（n = 11）训练至能完全负重行走（3 - 4周），另一组（假手术组；n = 7）未接受训练。在急性实验中，通过测量可乐定注射前后伸肌运动神经元的反应幅度，研究了I类通路、单突触兴奋、双突触抑制和多突触兴奋的变化。单突触兴奋未被可乐定改变，但因训练而显著降低。两组中可乐定都使双突触抑制显著降低，但在训练的猫中更显著，且在注射可乐定后训练使其进一步显著降低。此外，可乐定可使两组中的IB类抑制逆转为多突触兴奋，但在训练的猫中更频繁。我们还研究了虚拟踏步是否揭示了其他变化。在训练的猫中，所有三种反应的相位依赖性调制与先前报道的模式相似，但在假手术组中，单突触和多突触反应的调制并非如此。总体而言，训练似乎会降低单突触兴奋，并增强可乐定在减少双突触抑制和逆转为多突触兴奋方面的作用。因为人们认为多突触兴奋性I类通路将运动驱动传递至伸肌运动神经元，所以我们认为后一种变化将有助于在踏步过程中募集伸肌以恢复负重。
