ArticleThe Journal of general physiology2014
Nicotine exploits a COPI-mediated process for chaperone-mediated up-regulation of its receptors.
Article in The Journal of general physiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
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Who cites it
51 citing papers in PubMed, 75 citations in OpenAlex.
- Naltrexone, Naloxone, Morphine, and Fentanyl Pharmacologically Chaperone a Mutant μ-Opioid Receptor via an Endoplasmic Reticulum Exit Site-Dependent Pathway.Pharmacology research & perspectives · 2026Article
- Localization of Plasma Membrane and Intracellular Neuronal Nicotinic Acetylcholine Receptors Using Quantitative Imaging in Mammalian Cells.Journal of visualized experiments : JoVE · 2025Article
- Nicotinic Receptors in the Medial Habenula to Interpeduncular Nucleus Pathway: Modulators of Reward, Aversion and Emotion.The European journal of neuroscience · 2025Review
- Conditional knockout mouse model demonstrates that Copa expression is required for viability in development and adulthood.Biochemical and biophysical research communications · 2025Article
- Nicotine Attenuates Molecular Signalings in the BTBR TMolecular neurobiology · 2025Article
- Simulating early steps in nicotine dependence: Pharmacokinetics, activation, and chaperoning of nicotinic receptors.Molecular pharmacology · 2025Article
- Systemically circulating 17β-estradiol enhances the neuroprotective effect of the smoking cessation drug cytisine in female parkinsonian mice.NPJ Parkinson's disease · 2025Article
- Nicotine is an Immunosuppressant: Implications for Women's Health and Disease.Journal of neuroimmunology · 2024Review
- Article
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- Chemical Flavorants in Vaping Products Alter Neurobiology in a Sex-Dependent Manner to Promote Vaping-Related Behaviors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Protein profiling in the habenula after chronic (-)-menthol exposure in mice.Journal of neurochemistry · 2021Article
- Novel Putative Positive Modulators of α4β2 nAChRs Potentiate Nicotine Reward-Related Behavior.Molecules (Basel, Switzerland) · 2021Article
- Cytisine is neuroprotective in female but not male 6-hydroxydopamine lesioned parkinsonian mice and acts in combination with 17-β-estradiol to inhibit apoptotic endoplasmic reticulum stress in dopaminergic neurons.Journal of neurochemistry · 2021Article
- Nicotinic acetylcholine receptors and nicotine addiction: A brief introduction.Neuropharmacology · 2020Review
- The Impact of Electronic Nicotine Delivery System (ENDS) Flavors on Nicotinic Acetylcholine Receptors and Nicotine Addiction-Related Behaviors.Molecules (Basel, Switzerland) · 2020Review
- Brain Region-Specific nAChR and Associated Protein Abundance Alterations Following Chronic Nicotine and/or Menthol Exposure.Journal of proteome research · 2020Article
- Nicotinic Receptors Underlying Nicotine Dependence: Evidence from Transgenic Mouse Models.Current topics in behavioral neurosciences · 2020Article
- Why flavored vape products may be attractive: Green apple tobacco flavor elicits reward-related behavior, upregulates nAChRs on VTA dopamine neurons, and alters midbrain dopamine and GABA neuron function.Neuropharmacology · 2019Article
- Chronic Menthol Does Not Change Stoichiometry or Functional Plasma Membrane Levels of MouseMolecular pharmacology · 2019Article
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10 authors at 3 institutions in 1 country.
Funding
Abstract
Chronic exposure to nicotine up-regulates high sensitivity nicotinic acetylcholine receptors (nAChRs) in the brain. This up-regulation partially underlies addiction and may also contribute to protection against Parkinson's disease. nAChRs containing the α6 subunit (α6* nAChRs) are expressed in neurons in several brain regions, but comparatively little is known about the effect of chronic nicotine on these nAChRs. We report here that nicotine up-regulates α6* nAChRs in several mouse brain regions (substantia nigra pars compacta, ventral tegmental area, medial habenula, and superior colliculus) and in neuroblastoma 2a cells. We present evidence that a coat protein complex I (COPI)-mediated process mediates this up-regulation of α6* or α4* nAChRs but does not participate in basal trafficking. We show that α6β2β3 nAChR up-regulation is prevented by mutating a putative COPI-binding motif in the β3 subunit or by inhibiting COPI. Similarly, a COPI-dependent process is required for up-regulation of α4β2 nAChRs by chronic nicotine but not for basal trafficking. Mutation of the putative COPI-binding motif or inhibition of COPI also results in reduced normalized Förster resonance energy transfer between α6β2β3 nAChRs and εCOP subunits. The discovery that nicotine exploits a COPI-dependent process to chaperone high sensitivity nAChRs is novel and suggests that this may be a common mechanism in the up-regulation of nAChRs in response to chronic nicotine.
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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.