Pharmacological approach to the mechanisms of transcranial DC-stimulation-induced after-effects of human motor cortex excitability

被引:1017
作者
Liebetanz, D [1 ]
Nitsche, MA [1 ]
Tergau, F [1 ]
Paulus, W [1 ]
机构
[1] Univ Gottingen, Dept Clin Neurophysiol, D-37075 Gottingen, Germany
关键词
carbamazepine; dextromethorphan; neuroplasticity; transcranial direct current stimulation; transcranial magnetic stimulation;
D O I
10.1093/brain/awf238
中图分类号
R74 [神经病学与精神病学];
学科分类号
摘要
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.
引用
收藏
页码:2238 / 2247
页数:10
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