Department of Neuroscience, Medical University of South Carolina, Charleston, United States.
Center for Integrative Neuroscience, University of Tübingen, Tübingen, Germany.
Elife. 2019 Nov 5;8:e50855. doi: 10.7554/eLife.50855.
Cortical plasticity is fundamental to motor recovery following cortical perturbation. However, it is still unclear how this plasticity is induced at a functional circuit level. Here, we investigated motor recovery and underlying neural plasticity upon optogenetic suppression of a cortical area for eye movement. Using a visually-guided eye movement task in mice, we suppressed a portion of the secondary motor cortex (MOs) that encodes contraversive eye movement. Optogenetic unilateral suppression severely impaired contraversive movement on the first day. However, on subsequent days the suppression became inefficient and capability for the movement was restored. Longitudinal two-photon calcium imaging revealed that the regained capability was accompanied by an increased number of neurons encoding for ipsiversive movement in the unsuppressed contralateral MOs. Additional suppression of the contralateral MOs impaired the recovered movement again, indicating a compensatory mechanism. Our findings demonstrate that repeated optogenetic suppression leads to functional recovery mediated by the contralateral hemisphere.
皮质可塑性是皮质干扰后运动恢复的基础。然而，目前尚不清楚这种可塑性是如何在功能回路水平上诱导的。在这里，我们研究了光遗传学抑制眼球运动的皮质区域后运动恢复和潜在的神经可塑性。在小鼠的视觉引导眼球运动任务中，我们抑制了编码对侧眼球运动的次级运动皮质（MOs）的一部分。光遗传学单侧抑制在第一天严重损害了对侧运动。然而，在随后的几天里，抑制作用变得低效，运动能力得到恢复。纵向双光子钙成像显示，恢复的能力伴随着未受抑制的对侧 MOs 中编码同侧运动的神经元数量增加。对侧 MOs 的额外抑制再次损害了恢复的运动，表明存在代偿机制。我们的研究结果表明，重复的光遗传学抑制导致由对侧半球介导的功能恢复。
