Stefan Katja, Wycislo Matthias, Gentner Reinhard, Schramm Axel, Naumann Markus, Reiners Karlheinz, Classen Joseph
Human Cortical Physiology and Motor Control Laboratory, Department of Neurology, University of Würzburg, Josef-Schneider Strasse 11, D-97080 Würzburg, Germany.
Cereb Cortex. 2006 Mar;16(3):376-85. doi: 10.1093/cercor/bhi116. Epub 2005 Jun 1.
A novel Hebbian stimulation paradigm was employed to examine physiological correlates of motor memory formation in humans. Repetitive pairing of median nerve stimulation with transcranial magnetic stimulation over the contralateral motor cortex (paired associative stimulation, PAS) may decrease human motor cortical excitability at interstimulus intervals of 10 ms (PAS10) or increase excitability at 25 ms (PAS25). The properties of this plasticity have previously been shown to resemble associative timing-dependent long-term depression (LTD) and long-term potentiation (LTP) as established in vitro. Immediately after training a novel dynamic motor task, the capacity of the motor cortex to undergo plasticity in response to PAS25 was abolished. PAS10-induced plasticity remained unchanged. When retested after 6 h, PAS25-induced plasticity recovered to baseline levels. After training, normal PAS25-induced plasticity was observed in the contralateral training-naive motor cortex. Motor training did not reduce the efficacy of PAS25 to enhance cortical excitability when PAS10 was interspersed between the training and application of the PAS25 protocol. This indicated that the mechanism supporting PAS25-induced plasticity had remained intact immediately after training. Behavioral evidence was obtained for continued optimization of force generation at a time when PAS25-induced plasticity was blocked in the training motor cortex. Application of the PAS protocols after motor training did not prevent the consolidation of motor skills evident as performance gains at later retesting. The results are consistent with a concept of temporary suppression of associative cortical plasticity by neuronal mechanisms involved in motor training. Although it remains an open question exactly which element of motor training was responsible for this effect, our findings may link dynamic properties of LTP formation, as established in animal experiments, with human motor memory formation and possibly dynamic motor learning.
采用一种新型的赫布式刺激范式来研究人类运动记忆形成的生理相关性。将正中神经刺激与对侧运动皮层的经颅磁刺激进行重复配对（配对联想刺激，PAS），在10毫秒的刺激间隔（PAS10）下可能会降低人类运动皮层兴奋性，而在25毫秒时则会增加兴奋性（PAS25）。此前已表明，这种可塑性的特性类似于体外建立的联想时间依赖性长时程抑制（LTD）和长时程增强（LTP）。在训练一项新的动态运动任务后，运动皮层对PAS25产生可塑性的能力立即消失。PAS10诱导的可塑性保持不变。6小时后重新测试时，PAS25诱导的可塑性恢复到基线水平。训练后，在对侧未接受训练的运动皮层中观察到正常的PAS25诱导的可塑性。当在PAS25方案的训练和应用之间穿插PAS10时，运动训练并未降低PAS25增强皮层兴奋性的效果。这表明在训练后立即支持PAS25诱导可塑性的机制仍然完好无损。在训练的运动皮层中PAS25诱导的可塑性被阻断时，获得了行为证据，表明力量生成在持续优化。运动训练后应用PAS方案并不能阻止运动技能的巩固，这在后来的重新测试中表现为性能提高。这些结果与运动训练所涉及的神经元机制对联想性皮层可塑性的暂时抑制这一概念相一致。尽管究竟是运动训练的哪个因素导致了这种效应仍是一个悬而未决的问题，但我们的发现可能将动物实验中确立的LTP形成的动态特性与人类运动记忆形成以及可能的动态运动学习联系起来。
