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Live Imaging of Nicotine Induced Calcium Signaling and Neurotransmitter Release Along Ventral Hippocampal Axons
Published on: June 24, 2015
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Nicotine modulates human brain plasticity via calcium-dependent mechanisms
Jessica Grundey1, Jerick Barlay1, Giorgi Batsikadze1,2
1Department of Clinical Neurophysiology, University Medical Center, Georg-August-University, Göttingen, Germany.
The Journal of Physiology
|September 16, 2018
Summary
Nicotine impairs brain plasticity, but calcium channel blockers like flunarizine can restore it by regulating calcium levels. This finding is crucial for developing treatments for cognitive dysfunction.
Area of Science:
- Neuroscience
- Pharmacology
- Cognitive Science
Background:
- Nicotine (NIC) enhances cognition by modulating neurotransmitter systems and calcium permeability, crucial for learning and memory.
- NIC administration can impair calcium-dependent neuroplasticity induced by transcranial direct current stimulation (tDCS), potentially due to calcium overflow.
Purpose of the Study:
- To investigate the role of calcium in NIC's effects on tDCS-induced neuroplasticity.
- To determine if calcium channel blockade with flunarizine (FLU) can reverse NIC-induced impairment of neuroplasticity.
Main Methods:
- Healthy non-smokers received anodal tDCS combined with NIC patch and varying doses of FLU or placebo.
- Cortical excitability changes, indicative of long-term potentiation (LTP)-like plasticity, were measured.
Main Results:
- NIC abolished tDCS-induced neuroplasticity.
- Medium-dose FLU, combined with NIC, re-established plasticity.
- FLU alone showed dose-dependent effects, weakening or abolishing plasticity, with a medium dose inducing long-term depression-like plasticity.
Conclusions:
- Calcium influx and intracellular calcium levels play a critical role in NIC's modulation of LTP-like plasticity.
- Findings suggest a potential therapeutic window for NIC agonists in cognitive dysfunction, dependent on calcium regulation.
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