Pharmacological approach to the mechanisms of transcranial DC-stimulation-induced after-effects of human motor cortex excitability
Pharmacological approach to the mechanisms of transcranial DC-stimulation-induced after-effects of human motor cortex excitability
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DOI：
10.1093/brain/awf238
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发表时间：
2002-10-01
期刊：
影响因子：
14.5
通讯作者：
Paulus, W
中科院分区：
文献类型：
--
作者：
Liebetanz, D;Nitsche, MA;Paulus, W
弱经颅直流电刺激（tDCS）诱导人类运动皮层的持续兴奋性变化。这些可塑性兴奋性的变化是由刺激的极性、持续时间和电流强度选择性地控制的。为了揭示直流电（DC）诱导的神经可塑性的潜在机制，我们将运动皮层的tDCS与Na+通道阻断剂卡马西平（CBZ）和N-甲基-D-天冬氨酸（NMDA）受体拮抗剂二甲双胍（DMO）的应用相结合。通过经颅磁刺激（TMS），运动皮层兴奋性的变化高达40%，在无药物的条件下实现。阳极刺激可使皮层兴奋性增加，阴极刺激可使皮层兴奋性降低。这两种类型的兴奋性变化持续几分钟后停止电流刺激。DMO抑制了阳极和阴极DC刺激的后刺激效应，强烈表明NMDA受体参与了这两种类型的DC诱导的神经可塑性。相反，CBZ选择性消除阳极效应。由于CBZ稳定膜电位电压依赖性，结果表明，阳极tDCS的后效需要膜电位的去极化。类似的诱导建立类型的短期或长期的神经可塑性，一个相结合的神经递质和膜机制是必要的，以诱导tDCS的后效。在这些结果的基础上，我们认为，极性驱动的静息膜电位的改变代表了DC诱导的后效的关键机制，导致自发放电率的改变和NMDA受体激活的变化。
Weak transcranial direct current stimulation (tDCS) induces persisting excitability changes in the human motor cortex. These plastic excitability changes are selectively controlled by the polarity, duration and current strength of stimulation. To reveal the underlying mechanisms of direct current (DC)-induced neuroplasticity, we combined tDCS of the motor cortex with the application of Na+-channel-blocking carbamazepine (CBZ) and the N-methyl-D-aspartate (NMDA)-receptor antagonist dextromethorphan (DMO). Monitored by transcranial magnetic stimulation (TMS), motor cortical excitability changes of up to 40% were achieved in the drug-free condition. Increase of cortical excitability could be selected by anodal stimulation, and decrease by cathodal stimulation. Both types of excitability change lasted several minutes after cessation of current stimulation. DMO suppressed the post-stimulation effects of both anodal and cathodal DC stimulation, strongly suggesting the involvement of NMDA receptors in both types of DC-induced neuroplasticity. In contrast, CBZ selectively eliminated anodal effects. Since CBZ stabilizes the membrane potential voltage-dependently, the results reveal that after-effects of anodal tDCS require a depolarization of membrane potentials. Similar to the induction of established types of short- or long-term neuroplasticity, a combination of glutamatergic and membrane mechanisms is necessary to induce the after-effects of tDCS. On the basis of these results, we suggest that polarity-driven alterations of resting membrane potentials represent the crucial mechanisms of the DC-induced after-effects, leading to both an alteration of spontaneous discharge rates and to a change in NMDA-receptor activation.