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Anodal transcranial direct current stimulation (tDCS) over the primary motor cortex (M1) has been reported to increase the firing rates of neurons and to modulate the gamma-aminobutyric acid (GABA) concentration. To date, knowledge about the nature and duration of these tDCS induced effects is incomplete. We aimed to investigate long-term effects of anodal tDCS over M1 on GABA dynamics in humans. Repeated magnetic resonance spectroscopy (MRS) was employed to measure relative GABA concentration in M1 for approximately 64 minutes after stimulation. The study was performed on 32 healthy subjects. Either anodal or sham tDCS were applied for 10 minutes with the active electrode over the left M1 and the reference electrode over the right supra-orbital region. Pre and post-tDCS MRS scans were performed to acquire GABA-edited spectra using 3 T Prisma Siemens scanner. GABA signals showed no change over time in the sham tDCS group, whereas anodal tDCS resulted in a significant early decrease within 25 minutes after tDCS and then significant late decrease after 66 minutes which continued until the last test measurements. The late changes in GABA concentration might be related to long-term plasticity mechanism. These results contribute to a better understanding of the neurochemical mechanism underlying long-term cortical plasticity following anodal tDCS.

Nicotine modulates neuroplasticity and improves cognitive functions in animals and humans. In the brain of smoking individuals, calcium-dependent plasticity induced by non-invasive brain stimulation methods such as transcranial direct current stimulation (tDCS) and paired associative stimulation (PAS) is impaired by nicotine withdrawal, but partially re-established after nicotine re-administration. In order to investigate the underlying mechanism further, we tested the impact of the α4β2-nicotinic receptor partial agonist varenicline on focal and non-focal plasticity in smokers during nicotine withdrawal, induced by PAS and tDCS, respectively. We administered low (0.3 mg) and high (1.0 mg) single doses of varenicline or placebo medication before stimulation over the left motor cortex of 20 healthy smokers under nicotine withdrawal. Motor cortex excitability was monitored by single-pulse transcranial magnetic stimulation-induced motor evoked potential amplitudes for 36 hours after plasticity induction. Stimulation-induced plasticity was absent under placebo medication, whereas it was present in all conditions under high dose. Low dose restituted only tDCS-induced non-focal plasticity, producing no significant impact on focal plasticity. High dose varenicline also prolonged inhibitory plasticity. These results are comparable to the impact of nicotine on withdrawal-related impaired plasticity in smokers and suggest that α4β2 nicotinic receptors are relevantly involved in plasticity deficits and restitution in smokers. OA gold - CA extern