GABAergic modulation of DC stimulation-induced motor cortex excitability shifts in humans

Weak transcranial DC stimulation (tDCS) of the human motor cortex results in excitability shifts during and after the end of stimulation, which are most probably localized intracortically. Anodal stimulation enhances excitability, whereas cathodal stimulation reduces it. Although the after‐effects o...

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Bibliographic Details
Published in:The European journal of neuroscience 2004-05, Vol.19 (10), p.2720-2726
Main Authors: Nitsche, Michael A., Liebetanz, David, Schlitterlau, Anett, Henschke, Undine, Fricke, Kristina, Frommann, Kai, Lang, Nicolas, Henning, Stefan, Paulus, Walter, Tergau, Frithjof
Format: Article
Language:English
Subjects:
Adult
Analysis of Variance
Case-Control Studies
Electric Stimulation
Electrodes - classification
Electrodes - supply & distribution
Evoked Potentials, Motor - drug effects
Evoked Potentials, Motor - radiation effects
Female
GABA Modulators - pharmacology
Humans
lorazepam
Lorazepam - pharmacology
Magnetics
Male
Motor Cortex - drug effects
Motor Cortex - radiation effects
Neural Inhibition - drug effects
Neural Inhibition - radiation effects
neuroplasticity
Placebos - pharmacology
Random Allocation
Time Factors
transcranial direct current stimulation
transcranial magnetic stimulation
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Summary:Weak transcranial DC stimulation (tDCS) of the human motor cortex results in excitability shifts during and after the end of stimulation, which are most probably localized intracortically. Anodal stimulation enhances excitability, whereas cathodal stimulation reduces it. Although the after‐effects of tDCS are NMDA receptor‐dependent, nothing is known about the involvement of additional receptors. Here we show that pharmacological strengthening of GABAergic inhibition modulates selectively the after‐effects elicited by anodal tDCS. Administration of the GABAA receptor agonist lorazepam resulted in a delayed, but then enhanced and prolonged anodal tDCS‐induced excitability elevation. The initial absence of an excitability enhancement under lorazepam is most probably caused by a loss of the anodal tDCS‐generated intracortical diminution of inhibition and enhancement of facilitation, which occurs without pharmacological intervention. The reasons for the late‐occurring excitability enhancement remain unclear. Because intracortical inhibition and facilitation are not changed in this phase compared with pre‐tDCS values, excitability changes originating from remote cortical or subcortical areas could be involved.
ISSN:0953-816X
1460-9568
DOI:10.1111/j.0953-816X.2004.03398.x