Neuroscience Research Center, Healthy Ageing Research Center, and Department of Neurology, Chang Gung Memorial Hospital and Chang Gung University College of Medicine, Taoyuan, 33305, Taiwan.
Institute of Cognitive Neuroscience, National Central University, Taoyuan, 32001, Taiwan.
J Physiol. 2018 Sep;596(17):4207-4217. doi: 10.1113/JP276276. Epub 2018 Jul 5.
Synaptic plasticity is involved in daily activities but abnormal plasticity may be deleterious. In this study, we found that motor plasticity could be modulated by suppressing the premotor cortex with the theta burst form of repetitive transcranial magnetic stimulation. Such changes in motor plasticity were associated with reduced learning of a simple motor task. We postulate that the premotor cortex adjusts the amount of motor plasticity to modulate motor learning through heterosynaptic metaplasticity. The present results provide an insight into how the brain physiologically coordinates two different areas to bring them into a functional network, a concept that could be employed to intervene in diseases with abnormal plasticity.
Primary motor cortex (M1) plasticity is known to be influenced by the excitability and prior activation history of M1 itself. However, little is known about how its plasticity is influenced by other areas of the brain. In the present study on humans of either sex who were known to respond to theta burst stimulation from previous studies, we found plasticity of M1 could be modulated by suppressing the premotor cortex with the theta burst form of repetitive transcranial magnetic stimulation. Motor plasticity was distorted and disappeared 30 min and 120 min, respectively, after premotor excitability was suppressed. Further evaluation revealed that such changes in motor plasticity were associated with impaired learning of a simple motor task. We postulate that the premotor cortex modulates the amount of plasticity within M1 through heterosynaptic metaplasticity, and that this may impact on learning of a simple motor task previously shown to be directly affected by M1 plasticity. The present results provide an insight into how the brain physiologically coordinates two different areas to bring them into a functional network. Furthermore, such concepts could be translated into therapeutic approaches for diseases with aberrant plasticity.
突触可塑性参与日常活动，但异常的可塑性可能是有害的。在这项研究中，我们发现通过重复经颅磁刺激的θ爆发形式抑制运动前皮层可以调节运动可塑性。运动可塑性的这种变化与简单运动任务学习的减少有关。我们假设运动前皮层通过异突触代谢调节运动皮层的可塑性，从而调节运动学习。目前的结果提供了一个深入了解大脑如何通过生理协调两个不同区域来形成功能网络的概念，这一概念可用于干预具有异常可塑性的疾病。
初级运动皮层（M1）的可塑性已知受 M1 自身兴奋性和先前激活史的影响。然而，对于其可塑性如何受到大脑其他区域的影响知之甚少。在这项针对男女两性的研究中，已知他们对以前研究中的θ爆发刺激有反应，我们发现通过重复经颅磁刺激的θ爆发形式抑制运动前皮层可以调节 M1 的可塑性。在抑制运动前皮层兴奋性 30 分钟和 120 分钟后，分别观察到运动可塑性的扭曲和消失。进一步的评估表明，运动可塑性的这种变化与简单运动任务学习受损有关。我们假设运动前皮层通过异突触代谢调节 M1 内的可塑性程度，这可能会影响之前被认为直接受 M1 可塑性影响的简单运动任务的学习。目前的结果提供了一个深入了解大脑如何通过生理协调两个不同区域来形成功能网络的概念。此外，这些概念可以转化为治疗异常可塑性疾病的治疗方法。
