Abstract
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.
Highlights
Nicotine is the main psychoactive component of tobacco and responsible for its addictive properties [1]
With those differences in mind, we aimed to investigate the effect of nicotine spray on PAS25 induced long-term potentiation (LTP)-like motor cortex plasticity and Serial Reaction Time Task (SRTT) performance in deprived smokers
The results of the present study reveal that restitution of nicotine deprivation with nicotine spray in smokers has a prominent and rapid effect on paired associative stimulation (PAS)-25 induced excitatory neuroplasticity and SRTT performance
Summary
Nicotine is the main psychoactive component of tobacco and responsible for its addictive properties [1]. With non-invasive brain stimulation techniques like transcranial direct current stimulation (tDCS) and paired associative stimulation (PAS), cortical neuroplasticity can be examined in humans [10,11,12] Both protocols induce NMDA-receptor and calcium channel-dependent plasticity that are similar to long-term depression and LTP [13,14,15]. Nicotine spray on the other hand has a sharp rise and a slower decline in plasma levels, mimicking the pattern associated with smoking a cigarette [26] With those differences in mind, we aimed to investigate the effect of nicotine spray on PAS25 induced LTP-like motor cortex plasticity and Serial Reaction Time Task (SRTT) performance in deprived smokers. Based on the pharmacology and plasma levels reached with both application forms (nicotine spray and nicotine patch) (8–9 ng/ml), we hypothesized that nicotine spray is able to restore lacking LTP-like plasticity in deprived smokers and improves motor learning, similar to the impact of nicotine patch on brain physiology and cognitive performance
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