Pharmacological modulation of cortical excitability shifts induced by transcranial direct current stimulation in humans
Transcranial direct current stimulation (tDCS) of the human motor cortex results in polarity-specific shifts of cortical excitability during and after stimulation. Anodal tDCS enhances and cathodal stimulation reduces excitability. Animal experiments have demonstrated that the effect of anodal tDCS...
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Published in | The Journal of physiology Vol. 553; no. 1; pp. 293 - 301 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
The Physiological Society
15.11.2003
Blackwell Publishing Ltd Blackwell Science Inc |
Subjects | |
Online Access | Get full text |
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Summary: | Transcranial direct current stimulation (tDCS) of the human motor cortex results in polarity-specific shifts of cortical excitability
during and after stimulation. Anodal tDCS enhances and cathodal stimulation reduces excitability. Animal experiments have
demonstrated that the effect of anodal tDCS is caused by neuronal depolarisation, while cathodal tDCS hyperpolarises cortical
neurones. However, not much is known about the ion channels and receptors involved in these effects. Thus, the impact of the
sodium channel blocker carbamazepine, the calcium channel blocker flunarizine and the NMDA receptor antagonist dextromethorphane
on tDCS-elicited motor cortical excitability changes of healthy human subjects were tested. tDCS-protocols inducing excitability
alterations (1) only during tDCS and (2) eliciting long-lasting after-effects were applied after drug administration. Carbamazepine
selectively eliminated the excitability enhancement induced by anodal stimulation during and after tDCS. Flunarizine resulted
in similar changes. Antagonising NMDA receptors did not alter current-generated excitability changes during a short stimulation,
which elicits no after-effects, but prevented the induction of long-lasting after-effects independent of their direction.
These results suggest that, like in other animals, cortical excitability shifts induced during tDCS in humans also depend
on membrane polarisation, thus modulating the conductance of sodium and calcium channels. Moreover, they suggest that the
after-effects may be NMDA receptor dependent. Since NMDA receptors are involved in neuroplastic changes, the results suggest
a possible application of tDCS in the modulation or induction of these processes in a clinical setting. The selective elimination
of tDCS-driven excitability enhancements by carbamazepine proposes a role for this drug in focussing the effects of cathodal
tDCS, which may have important future clinical applications. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 |
ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1113/jphysiol.2003.049916 |