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Sci Rep. 2017 May 3;7(1):1387. doi: 10.1038/s41598-017-01428-6.

Compromised neuroplasticity in cigarette smokers under nicotine withdrawal is restituted by the nicotinic α4β2-receptor partial agonist varenicline.

Author information

1
Department of Clinical Neurophysiology, Georg-August-University of Göttingen, Robert Koch Straße 40, 37075, Göttingen, Germany.
2
Department of Neurology, Essen University Hospital, University of Duisburg-Essen, Hufelandstraße 55, 45147, Essen, Germany.
3
Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Nußbaumstraße 7, 80336, Munich, Germany.
4
Department of Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors, Ardeystraße 67, 44139, Dortmund, Germany.
5
Department of Psychology and Neurosciences, Leibniz Research Centre for Working Environment and Human Factors, Ardeystraße 67, 44139, Dortmund, Germany. nitsche@ifado.de.
6
Department of Neurology, University Medical Hospital Bergmannsheil, Bürkle de la Camp-Platz 1, 44789, Bochum, Germany. nitsche@ifado.de.

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.

PMID:
28469204
PMCID:
PMC5431184
DOI:
10.1038/s41598-017-01428-6
[Indexed for MEDLINE]
Free PMC Article

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