Nicotinic Restoration of Excitatory Neuroplasticity Is Linked to Improved Implicit Motor Learning Skills in Deprived Smokers.

Nicotine has been shown to modulate neuroplasticity, cognition, and learning processes in smokers and non-smokers. A possible mechanism for its effect on learning and memory formation is its impact on long-term depression and long-term potentiation (LTP). Nicotine abstinence in smokers is often correlated with impaired cognitive performance. As neuroplasticity is closely connected to learning and memory formation, we aimed to explore the effect of nicotine spray administration in deprived smokers on paired-associative stimulation (PAS25)-induced neuroplasticity and on performance of the serial reaction time task (SRTT), a sequential motor learning paradigm. Deprived smokers (n = 12) under placebo medication displayed reduced excitatory neuroplasticity induced by PAS25. Plasticity was restored by nicotine spray administration. Likewise, SRTT-performance improved after nicotine spray administration compared to placebo administration (n = 19). The results indicate a restitutional effect of nicotine spray in deprived smokers on both: LTP-like neuroplasticity and motor learning. These results present a possible explanation for persistence of nicotine addiction and probability of relapse.

Double dissociation of working memory and attentional processes in smokers and non-smokers with and without nicotine.

Nicotine has been shown to affect cortical excitability measured using transcranial magnetic stimulation in smoking and non-smoking subjects in different ways. In tobacco-deprived smokers, administration of nicotine restores compromised cortical facilitation while in non-smokers, it enhances cortical inhibition. As cortical excitability and activity are closely linked to cognitive processes, we aimed to explore whether nicotine-induced physiological alterations in non-smokers and smokers are associated with cognitive changes. Specifically, we assessed the impact of nicotine on working memory performance (n-back letter task) and on attentional processes (Stroop interference test) in healthy smokers and non-smokers. Both tasks have been shown to rely on prefrontal areas, and nicotinic receptors are relevantly involved in prefrontal function. Sixteen smoking and 16 non-smoking subjects participated in the 3-back letter task and 21 smoking and 21 non-smoking subjects in the Stroop test after the respective application of placebo or nicotine patches. The results show that working memory and attentional processes are compromised in nicotine-deprived smokers compared to non-smoking individuals. After administration of nicotine, working memory performance in smokers improved, while non-smoking subjects displayed decreased accuracy with increased number of errors. The effects have been shown to be more apparent for working memory performance than attentional processes. In summary, cognitive functions can be restored by nicotine in deprived smokers, whereas non-smokers do not gain additional benefit. The respective changes are in accordance with related effects of nicotine on cortical excitability in both groups.