NMDA Receptor-Mediated Motor Cortex Plasticity After 20 Hz Transcranial Alternating Current Stimulation.
M Wischnewski1,2, M Engelhardt2, M A Salehinejad2
1Donders Centre for Cognition, Donders Institute, Radboud University, Nijmegen, The Netherlands.
Cerebral Cortex (New York, N.Y. : 1991)
|July 12, 2018
Summary
Transcranial alternating current stimulation (tACS) enhances motor cortex activity and oscillations. This effect relies on N-methyl-d-aspartate receptors (NMDARs), demonstrating tACS-induced plasticity in the human motor cortex.
Area of Science:
- Neuroscience
- Motor Cortex Physiology
- Synaptic Plasticity
Background:
- Transcranial alternating current stimulation (tACS) modulates neural oscillations and excitability in the primary motor cortex (M1).
- tACS after-effects suggest a role for N-methyl-d-aspartate receptor (NMDAR) mediated synaptic plasticity, but underlying cortical mechanisms remain unexplored.
Purpose of the Study:
- To investigate the cortical mechanisms behind tACS after-effects in the primary motor cortex (M1).
- To determine if NMDARs mediate the prolonged effects of tACS on motor cortex excitability and oscillations.
Main Methods:
- Applied 20 Hz beta tACS to the primary motor cortex (M1).
- Administered either the NMDAR antagonist dextromethorphan or a placebo to participants.
- Measured effects on cortical beta oscillations and M1 excitability.
Main Results:
- In the placebo condition, beta tACS increased M1 excitability and beta oscillations for at least 60 minutes.
- When dextromethorphan was administered, these tACS-induced effects were completely abolished.
- This indicates NMDARs are crucial for tACS after-effects.
Conclusions:
- Provides the first direct evidence that tACS induces NMDAR-mediated plasticity in the human motor cortex.
- Enhances understanding of the physiological mechanisms underlying tACS effects on motor cortex function.
- Highlights the role of synaptic plasticity in tACS-induced neuromodulation.
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