Department of Neurophysiology, Nencki Institute of Experimental Biology, Warsaw, Poland.
Eur J Neurosci. 2012 Sep;36(5):2679-88. doi: 10.1111/j.1460-9568.2012.08182.x. Epub 2012 Jun 19.
Cholinergic input modulates excitability of motoneurons and plays an important role in the control of locomotion in both intact and spinalized animals. However, spinal cord transection in adult rats affects cholinergic innervation of only some hindlimb motoneurons, suggesting that specificity of this response is related to functional differences between motoneurons. Our aim was therefore to compare cholinergic input to motoneurons innervating the soleus (Sol) and tibialis anterior (TA) motoneurons following spinal cord transection at a low-thoracic level. The second aim was to investigate whether deficits in cholinergic input to these motoneurons could be modified by locomotor training. The Sol and TA motoneurons were identified by retrograde labelling with fluorescent dyes injected intramuscularly. Cholinergic terminals were detected using anti-vesicular acetylcholine transporter (VAChT) antibody. Overall innervation of motoneurons was evaluated with anti-synaptophysin antibody. After spinalization we found a decrease in the number of VAChT-positive boutons apposing perikarya of the Sol (to 49%) but not TA motoneurons. Locomotor training, resulting in moderate functional improvement, partly reduced the deficit in cholinergic innervation of Sol motoneurons by increasing the number of VAChT-positive boutons. However, the optical density of VAChT-positive boutons terminating on various motoneurons, which decreased after spinalization, continued to decrease despite the training, suggesting an impairment of acetylcholine availability in the terminals. Different effects of spinal cord transection on cholinergic innervation of motoneurons controlling the ankle extensor and flexor muscles point to different functional states of these muscles in paraplegia as a possible source of activity-dependent signaling regulating cholinergic input to the motoneurons.
胆碱能输入调节运动神经元的兴奋性，在完整和脊髓切断动物的运动控制中发挥重要作用。然而，成年大鼠脊髓切断仅影响部分后肢运动神经元的胆碱能神经支配，这表明这种反应的特异性与运动神经元之间的功能差异有关。因此，我们的目的是比较脊髓切断后低胸段对支配比目鱼肌（Sol）和胫骨前肌（TA）运动神经元的运动神经元的胆碱能输入。第二个目的是研究这些运动神经元的胆碱能输入缺陷是否可以通过运动训练来改变。通过肌肉内注射荧光染料进行逆行标记来鉴定 Sol 和 TA 运动神经元。使用抗囊泡乙酰胆碱转运蛋白（VAChT）抗体检测胆碱能终末。用抗突触素抗体评估运动神经元的整体神经支配。脊髓切断后，我们发现 Sol 运动神经元的 VAChT 阳性终末数量减少（至 49%），但 TA 运动神经元没有减少。运动训练导致适度的功能改善，部分减少了 Sol 运动神经元胆碱能神经支配的缺陷，增加了 VAChT 阳性终末的数量。然而，VAChT 阳性终末在各种运动神经元上的光密度在脊髓切断后下降，尽管进行了训练，但仍继续下降，表明末端乙酰胆碱的可用性受损。控制踝关节伸肌和屈肌的运动神经元的胆碱能传入对脊髓切断的不同影响表明，截瘫中这些肌肉的不同功能状态可能是调节运动神经元胆碱能传入的活动依赖性信号的来源。
