ArticleThe Journal of physiology2018
Nicotine modulates human brain plasticity via calcium-dependent mechanisms.
Article in The Journal of physiology, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers, 2 of them syntheses that pooled it.
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Who cites it
16 citing papers in PubMed, 2 syntheses or guidelines pooled it, 34 citations in OpenAlex.
- Meta-analysis of variance in tDCS effects on response inhibition.Scientific reports · 2024Pooled it
- The two-way relationship between nicotine and cortical activity: a systematic review of neurobiological and treatment aspects.European archives of psychiatry and clinical neuroscience · 2021Pooled it
- Expanding the parameter space of anodal transcranial direct current stimulation of the primary motor cortex.Scientific reports · 2019Trial
- Prefrontal TDCS does not improve working memory performance in individuals with chronic alcohol and tobacco use.IBRO neuroscience reports · 2026Article
- Investigating the Potential Roles of Environmental Exposures on the Pathology of Amyotrophic Lateral Sclerosis by Overlap Analysis.Neurotoxicity research · 2025Article
- Gating of Neuroplasticity: Effects and Mechanisms of Acute Aerobic Exercise as a Brain Stimulation for the Sensorimotor Cortex.Advances in neurobiology · 2025Review
- Article
- A study of long-term GABA and high-energy phosphate alterations in the primary motor cortex using anodal tDCS andFrontiers in human neuroscience · 2024Article
- Inhibitory Control in Young Healthy Adults - a tDCS Study.Physiological research · 2023Article
- NMDA receptor-related mechanisms of dopaminergic modulation of tDCS-induced neuroplasticity.Cerebral cortex (New York, N.Y. : 1991) · 2022Article
- Article
- Inter-Individual Variability in tDCS Effects: A Narrative Review on the Contribution of Stable, Variable, and Contextual Factors.Brain sciences · 2022Review
- Consequences of prefrontal tDCS on inhibitory control and reactive aggression.Social cognitive and affective neuroscience · 2022Article
- Nicotine Facilitates Facial Stimulation-Evoked Mossy Fiber-Granule Cell Long-Term PotentiationFrontiers in cellular neuroscience · 2022Article
- Neuromodulating the performance monitoring network during conflict and error processing in healthy populations: Insights from transcranial electric stimulation studies.Frontiers in integrative neuroscience · 2022Review
- Functional alterations by a subgroup of neonicotinoid pesticides in human dopaminergic neurons.Archives of toxicology · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
key pointsNicotine (NIC) modulates cognition and memory function by targeting the nicotinic ACh receptor and releasing different transmitter systems postsynaptically. With both NIC-generated mechanisms, calcium influx and calcium permeability can be regulated, which is a key requirement for the induction of long-term potentiation, comprising the physiological basis of learning and memory function. We attempt to unmask the underlying mechanism of nicotinic effects on anodal transcranial direct current stimulation (tDCS)-induced long-term potentiation-like plasticity based on the hypothesis of calcium-dependency. Abolished tDCS-induced neuroplasticity as a result of NIC administration is reversed by calcium channel blockade with flunarizine in a dose-dependent manner. The results of the present study suggest that there is a dose determination of NIC/NIC agonists in therapeutical settings when treating cognitive dysfunction, which partially explains the heterogeneous results on cognition observed in subjects in different experimental settings. ABSTRACT: Nicotine (NIC) modulates neuroplasticity and improves cognitive performance in animals and humans mainly by increased calcium permeability and modulation of diverse transmitter systems. NIC administration impairs calcium-dependent plasticity induced by non-invasive brain stimulation with transcranial direct current stimulation (tDCS) in non-smoking participants probably as a result of intracellular calcium overflow. To test this hypothesis, we analysed the effect of calcium channel blockade with flunarizine (FLU) on anodal tDCS-induced cortical excitability changes in healthy non-smokers under NIC. We applied anodal tDCS combined with NIC patch and FLU at three different doses (2.5, 5 and 10 mg) or with placebo medication. NIC abolished anodal tDCS-induced neuroplasticity. Under medium dosage (but not under low and high dosage) of FLU combined with NIC, plasticity was re-established. For FLU alone, the lowest dosage weakened long-term potentiation (LTP)-like plasticity, whereas the highest dosage again abolished tDCS-induced plasticity. The medium dosage turned LTP-like plasticity in long-term depression-like plasticity. The results of the present study suggest a key role of calcium influx and calcium levels in nicotinic effects on LTP-like plasticity in humans. This knowledge might be relevant for the development of new therapeutic strategies in cognitive dysfunction.
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