Département de Neurosciences Groupe de recherche sur le système nerveux central (GRSNC) and Centre Interdisciplinaire de Recherche sur le Cerveau au service de l'Apprentissage (CIRCA), Université de Montréal, Québec, Canada; CIUSSS du Nord-de-l'Île-de-Montréal, Québec, Canada.
Département de Neurosciences Groupe de recherche sur le système nerveux central (GRSNC) and Centre Interdisciplinaire de Recherche sur le Cerveau au service de l'Apprentissage (CIRCA), Université de Montréal, Québec, Canada; CIUSSS du Nord-de-l'Île-de-Montréal, Québec, Canada.
Exp Neurol. 2021 Sep;343:113775. doi: 10.1016/j.expneurol.2021.113775. Epub 2021 May 31.
After incomplete spinal cord injury (SCI), cortical plasticity is involved in hindlimb locomotor recovery. Nevertheless, whether cortical activity is required for motor map plasticity and recovery remains unresolved. Here, we combined a unilateral thoracic spinal cord injury (SCI) with a cortical inactivation protocol that uncovered a functional role of contralesional cortical activity in hindlimb recovery and ipsilesional map plasticity. In adult rats, left hindlimb paralysis was induced by sectioning half of the spinal cord at the thoracic level (hemisection) and we used a continuous infusion of muscimol (GABA agonist, 10 mM, 0.11 µl/h) delivered via implanted osmotic pump (n = 9) to chronically inactivate the contralesional hindlimb motor cortex. Hemisected rats with saline infusion served as a SCI control group (n = 8), and intact rats with muscimol infusion served as an inactivation control group (n = 6). Locomotion was assessed in an open field, on a horizontal ladder, and on a treadmill prior to and for three weeks after hemisection. Cortical inactivation after hemisection significantly impeded hindlimb locomotor recovery in all tasks and specifically disrupted the ability of rats to generate proper flexion of the affected hindlimb during stepping compared to SCI controls, with no significant effect of inactivation in intact rats. Chronic and acute (n = 4) cortical inactivation after hemisection also significantly reduced the representation of the affected hindlimb in the ipsilesional motor cortex derived with intracortical microsimulation (ICMS). Our results provide evidence that residual activity in the contralesional hindlimb motor cortex after thoracic hemisection contributes to spontaneous locomotor recovery and map plasticity.
不完全性脊髓损伤（SCI）后，皮质可塑性参与后肢运动恢复。然而，皮质活动是否需要运动图的可塑性和恢复仍未解决。在这里，我们将单侧胸段脊髓损伤（SCI）与皮质失活方案相结合，揭示了对侧皮质活动在后肢恢复和同侧图可塑性中的功能作用。在成年大鼠中，通过在胸段（半切）处横断脊髓的一半来诱导左后肢麻痹，我们使用通过植入的渗透泵（n=9）递送的持续 10 mM 肌肉碱（GABA 激动剂，0.11 µl/h）输注来慢性失活对侧后肢运动皮质。接受盐水输注的半切大鼠作为 SCI 对照组（n=8），接受肌肉碱输注的完整大鼠作为失活对照组（n=6）。在半切之前和之后的三周，在开放场、水平梯和跑步机上评估运动。半切后皮质失活显著阻碍了所有任务中的后肢运动恢复，特别是与 SCI 对照组相比，大鼠在步幅中产生受影响后肢适当弯曲的能力受到破坏，而在完整大鼠中，失活没有显著影响。半切后慢性和急性（n=4）皮质失活也显著降低了经皮内微刺激（ICMS）获得的同侧运动皮质中受影响后肢的代表性。我们的结果提供了证据，表明胸段半切后对侧后肢运动皮质中的残留活动有助于自发性运动恢复和图的可塑性。
