ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2004
Nicotine enhancement of dopamine release by a calcium-dependent increase in the size of the readily releasable pool of synaptic vesicles.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.
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Who cites it
37 citing papers in PubMed, 72 citations in OpenAlex.
- Cortical excitability in smoking and not smoking individuals with and without nicotine.Psychopharmacology · 2013Trial
- Proposed mechanisms of neuroprotection for nicotine in Parkinson's disease.Journal of Parkinson's disease · 2025Review
- Erasing "bad memories": reversing aberrant synaptic plasticity as therapy for neurological and psychiatric disorders.Molecular psychiatry · 2025Review
- Role of extracellular vesicle-mediated neurodegeneration in substance use disorders.Current opinion in physiology · 2025Article
- Restoration of MPTP-induced Dopamine and Tyrosine Hydroxylase Depletion in the Mouse Brain Through Ethanol and Nicotine.Neurotoxicity research · 2025Article
- Transcranial Direct Current Stimulation to Ameliorate Post-Stroke Cognitive Impairment.Brain sciences · 2024Review
- Synaptic Vesicle Glycoprotein 2C: a role in Parkinson's disease.Frontiers in cellular neuroscience · 2024Review
- Axonal α7* nicotinic acetylcholine receptors modulate glutamatergic signaling and synaptic vesicle organization in ventral hippocampal projections.Frontiers in neural circuits · 2022Article
- Activation of β3-adrenoceptor increases the number of readily releasable glutamatergic vesicle via activating CaScientific reports · 2021Article
- Spatial and temporal scales of dopamine transmission.Nature reviews. Neuroscience · 2021Review
- Endocannabinoid Modulation of Nucleus Accumbens Microcircuitry and Terminal Dopamine Release.Frontiers in synaptic neuroscience · 2021Review
- Direct dopamine terminal regulation by local striatal microcircuitry.Journal of neurochemistry · 2020Review
- Nicotinic acetylcholine receptors regulate clustering, fusion and acidification of the rat brain synaptic vesicles.Neurochemistry international · 2020Article
- Does kynurenic acid act on nicotinic receptors? An assessment of the evidence.Journal of neurochemistry · 2020Review
- Electrochemical Measurements of Acetylcholine-Stimulated Dopamine Release in Adult Drosophila melanogaster Brains.Analytical chemistry · 2018Article
- Computational modeling and biomarker studies of pharmacological treatment of Alzheimer's disease (Review).Molecular medicine reports · 2018Review
- Neuregulin 3 Signaling Mediates Nicotine-Dependent Synaptic Plasticity in the Orbitofrontal Cortex and Cognition.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2018Article
- To Do or Not to Do: Dopamine, Affordability and the Economics of Opportunity.Frontiers in integrative neuroscience · 2018Article
- Article
- Neurotensinergic augmentation of glutamate release at the perforant path-granule cell synapse in rat dentate gyrus: Roles of L-Type Ca²⁺ channels, calmodulin and myosin light-chain kinase.Neuropharmacology · 2015Article
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A major factor underlying compulsive tobacco use is nicotine-induced modulation of dopamine release in the mesolimbic reward pathway (Wise and Rompre, 1989). An established biochemical mechanism for nicotine-enhanced dopamine release is by activating presynaptic nicotinic acetylcholine receptors (nAChRs) (Wonnacott, 1997). Prolonged application of 10(-7) to 10(-5) m nicotine to striatal synaptosomes promoted a sustained efflux of [3H]dopamine. This nicotine effect was mediated by non-alpha7 nAChRs, because it was blocked by 5 mum mecamylamine but was resistant to 100 nm alpha-bungarotoxin (alphaBgTx). Dopamine release was diminished by omitting Na+ or by applying peptide calcium channel blockers, indicating that nAChRs trigger release by depolarizing the nerve terminals. However, because alpha7 receptors rapidly desensitize in the continuous presence of agonists, a repetitive stimulation protocol was used to evaluate the possible significance of desensitization. This protocol produced a transient increase in [3H]dopamine released by depolarization and a significant increase in the response to hypertonic solutions that measure the size of the readily releasable pool (RRP) of synaptic vesicles. The nicotine-induced increase in the size of the readily releasable pool was blocked by alphaBgTx and by the calmodulin antagonist calmidazolium, suggesting that Ca2+ entry through alpha7 nAChRs specifically enhances synaptic vesicle mobilization at dopamine terminals. Thus, nicotine enhances dopamine release by two complementary actions mediated by discrete nAChR subtypes and suggest that the alpha7 nAChR-mediated pathway is tightly and specifically coupled to refilling of the RRP of vesicles in dopamine terminals.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.