ArticleThe Journal of pharmacology and experimental therapeutics2009
Cocaine alters vesicular dopamine sequestration and potassium-stimulated dopamine release: the role of D2 receptor activation.
Article in The Journal of pharmacology and experimental therapeutics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 23 citations in OpenAlex.
- Disruption of Dopamine Homeostasis by Psychostimulants.Molecular neurobiology · 2026Review
- Fiber Photometry Analysis of Spontaneous Dopamine Signals: TheACS chemical neuroscience · 2025Article
- Kappa opioid receptors diminish spontaneous dopamine signals in awake mice through multiple mechanisms.Neuropharmacology · 2025Article
- Fiber photometry analysis of spontaneous dopamine signals: The z-scored data are not the data.bioRxiv : the preprint server for biology · 2025Article
- Kappa Opioid Receptors Negatively Regulate Real Time Spontaneous Dopamine Signals by Reducing Release and Increasing Uptake.bioRxiv : the preprint server for biology · 2024Article
- Vesicular monoamine transporter (VMAT) regional expression and roles in pathological conditions.Heliyon · 2023Review
- Interactions of calmodulin kinase II with the dopamine transporter facilitate cocaine-induced enhancement of evoked dopamine release.Translational psychiatry · 2023Article
- 3,4-Methylenedioxypyrovalerone: Neuropharmacological Impact of a Designer Stimulant of Abuse on Monoamine Transporters.The Journal of pharmacology and experimental therapeutics · 2020Article
- Combined Amperometry and Electrochemical Cytometry Reveal Differential Effects of Cocaine and Methylphenidate on Exocytosis and the Fraction of Chemical Release.Angewandte Chemie (International ed. in English) · 2019Article
- Lipid peroxidation and apoptotic response in rat brain areas induced by long-term administration of nandrolone: the mutual crosstalk between ROS and NF-kB.Journal of cellular and molecular medicine · 2016Article
- Modulating dopamine release by optogenetics in transgenic mice reveals terminal dopaminergic dynamics.Neurophotonics · 2015Article
- Advances in studying phasic dopamine signaling in brain reward mechanisms.Frontiers in bioscience (Elite edition) · 2013Review
- Chronic pre-exposure to methamphetamine following 31 days of withdrawal impairs sexual performance but not sexual conditioning in male Japanese quail.Behavioural processes · 2012Article
- Cocaine self-administration produces pharmacodynamic tolerance: differential effects on the potency of dopamine transporter blockers, releasers, and methylphenidate.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012Article
- Vesicular and plasma membrane transporters for neurotransmitters.Cold Spring Harbor perspectives in biology · 2012Review
- Monoamine transporters: vulnerable and vital doorkeepers.Progress in molecular biology and translational science · 2011Review
- Methamphetamine alters vesicular monoamine transporter-2 function and potassium-stimulated dopamine release.Journal of neurochemistry · 2010Article
- Measurement of plasmalemmal dopamine transport, vesicular dopamine transport, and K(+)-stimulated dopamine release in frozen rat brain tissue.Journal of neuroscience methods · 2009Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Cocaine is a psychostimulant that inhibits the inward transport of dopamine (DA) via the neuronal DA transporter, thereby increasing DA concentrations in the synaptic cleft. Cocaine administration also causes a redistribution of striatal vesicular monoamine transporter (VMAT)-2-containing vesicles that co-fractionate with synaptosomal membranes after osmotic lysis (referred to herein as membrane-associated vesicles) to a nonmembrane-associated, cytoplasmic subcellular fraction. Although previous studies from our laboratory have focused on the impact of cocaine on cytoplasmic vesicles, the present report describes the pharmacological effects of cocaine on the membrane-associated vesicle population. Results revealed that the redistribution of VMAT-2 and associated vesicles away from synaptosomal membranes is associated with a decrease in total DA transport and DA content in the membrane-associated VMAT-2-containing subcellular fraction. Cocaine also decreases the velocity and magnitude of K+-stimulated exocytotic DA release from whole striatal suspensions. The cocaine-induced VMAT-2 redistribution, decrease in DA release, and decrease in total DA transport are mediated by D2 receptors as these events were prevented by pretreatment with the D2 receptor antagonist, eticlopride [S-(-)-3-chloro-5-ethyl-N-[(1-ethyl-2-pyrrolidinyl)methyl]-6-hydroxy-2-methoxybenzamide hydrochloride]. These data suggest that after cocaine administration, D2 receptors are activated because of increased synaptic DA, resulting in a redistribution of DA-containing vesicles away from synaptosomal membranes, thus leading to less DA released after a depolarizing stimulus. These findings provide insight into not only the mechanism of action of cocaine but also mechanisms underlying the regulation of dopaminergic neurons.
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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.