Abstract
In various studies nicotine has shown to alter cognitive functions in non-smoking subjects. The physiological basis for these effects might be nicotine-generated modulation of cortical structure, excitability, and activity, as mainly described in animal experiments. In accordance, a recently conducted study demonstrated that application of nicotine for hours via nicotine patch in non-smoking humans alters the effects of neuroplasticity-inducing non-invasive brain stimulation techniques on cortical excitability. Specifically, nicotine abolished inhibitory plasticity independent from the focality of the stimulation protocol. While nicotine prevented also the establishment of non-focal facilitatory plasticity, focal synapse-specific facilitatory plasticity was enhanced. These results agree with a focusing effect of prolonged nicotine application on facilitatory plasticity. However, since nicotine induces rapid adaption processes of its receptors, this scenario might differ from the effect of nicotine in cigarette smoking. Thus in this study we aimed to gain further insight in the mechanism of nicotine on plasticity by exploring the effect of nicotine spray on non-focal and focal plasticity-inducing protocols in non-smoking subjects, a fast-acting agent better comparable to cigarette smoking. Focal, synapse-specific plasticity was induced by paired associative stimulation (PAS), while non-focal plasticity was elicited by transcranial direct current stimulation (tDCS). Forty eight non-smokers received nicotine spray respectively placebo combined with one of the following protocols (anodal tDCS, cathodal tDCS, PAS-25, and PAS-10). Corticospinal excitability was monitored via motor-evoked potentials elicited by transcranial magnetic stimulation (TMS). Nicotine spray abolished facilitatory plasticity irrespective of focality and PAS-10-induced excitability diminution, while tDCS-derived excitability reduction was delayed and weakened. Nicotine spray had thus a clear effect on neuroplasticity in non-smoking subjects. However, the effects of nicotine spray differ clearly from those of prolonged nicotine application, which might be due to missing adaptive nicotinic receptor alterations. These results enhance our knowledge about the dynamic impact of nicotine on plasticity, which might be related to its heterogenous effect on cognition.
Highlights
Nicotine binds to the nicotinergic type of cholinergic receptors, which are ligand-gated cation channels
No significant group differences were found in terms of age, gender, transcranial magnetic stimulation (TMS)-intensity to elicit an motor-evoked potentials (MEPs) of 1 mV (S1 mV) before and after administration of nicotine spray
EFFECTS OF NICOTINE SPRAY ON transcranial direct current stimulation (tDCS)-INDUCED PLASTICITY IN NON-SMOKERS In the PLC condition the anodal tDCS-induced excitability increased MEP amplitudes stayed significant until 90 min after stimulation, and the cathodal tDCS-induced inhibition lasted until 90 min after tDCS
Summary
Nicotine binds to the nicotinergic type of cholinergic receptors, which are ligand-gated cation channels. Hereby nicotine is thought to be critically involved in the induction and modulation of neuroplasticity (Burnashev, 1998; Dajas-Bailador and Wonnacott, 2004; Levin et al, 2006), the likely physiological basis of learning and memory formation (Rioult-Pedotti et al, 1998, 2000). COGNITIVE EFFECTS OF NICOTINE On a functional basis, in animal experiments nicotine has been shown to improve working memory function (Levin et al, 1994). Kleykamp et al (2005) have found no effect of nicotine gum in different doses on attention and working memory in never-smokers. Other studies have shown that nicotine improves alerting attention-accuracy (Barr et al, 2008), visuospatial attention (Thiel et al, 2005), and working memory (Kumari et al, 2003) in non-smoking subjects. Nicotinic plasticity modulation has been explored only in few studies in humans so far
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