Catecholaminergic consolidation of motor cortical neuroplasticity in humans

Cereb Cortex. 2004 Nov;14(11):1240-5. doi: 10.1093/cercor/bhh085. Epub 2004 May 13.

Abstract

Amphetamine, a catecholaminergic re-uptake-blocker, is able to improve neuroplastic mechanisms in humans. However, so far not much is known about the underlying physiological mechanisms. Here, we study the impact of amphetamine on NMDA receptor-dependent long-lasting excitability modifications in the human motor cortex elicited by weak transcranial direct current stimulation (tDCS). Amphetamine significantly enhanced and prolonged increases in anodal, tDCS-induced, long-lasting excitability. Under amphetamine premedication, anodal tDCS resulted in an enhancement of excitability which lasted until the morning after tDCS, compared to approximately 1 h in the placebo condition. Prolongation of the excitability enhancement was most pronounced for long-term effects; the duration of short-term excitability enhancement was only slightly increased. Since the additional application of the NMDA receptor antagonist dextromethorphane blocked any enhancement of tDCS-driven excitability under amphetamine, we conclude that amphetamine consolidates the tDCS-induced neuroplastic effects, but does not initiate them. The fact that propanolol, a beta-adrenergic antagonist, diminished the duration of the tDCS-generated after-effects suggests that adrenergic receptors play a certain role in the consolidation of NMDA receptor-dependent motor cortical excitability modifications in humans. This result may enable researchers to optimize neuroplastic processes in the human brain on the rational basis of purpose-designed pharmacological interventions.

Publication types

  • Comparative Study
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adult
  • Amphetamine / pharmacology
  • Analysis of Variance
  • Catecholamines / physiology*
  • Evoked Potentials, Motor / drug effects
  • Evoked Potentials, Motor / physiology*
  • Female
  • Humans
  • Male
  • Motor Cortex / drug effects
  • Motor Cortex / physiology*
  • Neuronal Plasticity / drug effects
  • Neuronal Plasticity / physiology*

Substances

  • Catecholamines
  • Amphetamine