Abstract
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.
Highlights
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 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 transcranial direct current stimulation (tDCS), respectively
Summary
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. Experiments in humans have shown that both, nicotine-induced non-selective activation of nAChRs, and targeted α4β2 and α7 receptor activation by respective agonists result in an increase of focal plasticity, while abolishing the effects of more diffuse plasticity induction protocols in non-smokers[11, 12]. Plasticity in the above-mentioned studies was induced by non-invasive brain stimulation protocols, such as transcranial direct current stimulation (tDCS) and paired associative stimulation (PAS) Both techniques induce long-lasting Ca2+- and NMDA receptor-dependent shifts in cortical excitability . For tDCS, LTP-like plasticity is induced by anodal, and LTD-like plasticity by cathodal stimulation of the target area[16], while for PAS synchrony of activation of somatosensory-motor cortical connections determines plasticity direction, resembling spike-timing dependent plasticity[15]
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