ArticleJournal of neurochemistry2010
Methamphetamine alters vesicular monoamine transporter-2 function and potassium-stimulated dopamine release.
Article in Journal of neurochemistry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
14 citing papers in PubMed, 29 citations in OpenAlex.
- Interactions of VMAT2 with CDCrel-1 and Parkin in Methamphetamine Neurotoxicity.International journal of molecular sciences · 2024Article
- Impact of HIV-1 tat protein on methamphetamine-induced inhibition of vesicular monoamine transporter2-mediated dopamine transport and methamphetamine conditioned place preference in HIV-1 tat transgenic mice.European journal of pharmacology · 2024Article
- Transient receptor potential ankyrin 1 channel modulates the abuse-related mechanisms of methamphetamine through interaction with dopamine transporter.British journal of pharmacology · 2024Article
- Neurotoxic Methamphetamine Doses Alter CDCel-1 Levels and Its Interaction with Vesicular Monoamine Transporter-2 in Rat Striatum.bioRxiv : the preprint server for biology · 2024Article
- N-Isopropylbenzylamine-induced conditioned place preference, sensitization behaviour and self-administration in rodents.Addiction biology · 2024Article
- A history of ethanol drinking increases locomotor stimulation and blunts enhancement of dendritic dopamine transmission by methamphetamine.Addiction biology · 2020Article
- The Role of Biogenic Amine Transporters in Trace Amine-Associated Receptor 1 Regulation of Methamphetamine-Induced Neurotoxicity.The Journal of pharmacology and experimental therapeutics · 2019Article
- Regulation of the Dopamine and Vesicular Monoamine Transporters: Pharmacological Targets and Implications for Disease.Pharmacological reviews · 2015Review
- Prior methamphetamine self-administration attenuates the dopaminergic deficits caused by a subsequent methamphetamine exposure.Neuropharmacology · 2015Article
- The vesicular monoamine transporter 2: an underexplored pharmacological target.Neurochemistry international · 2014Review
- A fluorescent-based assay for live cell, spatially resolved assessment of vesicular monoamine transporter 2-mediated neurotransmitter transport.Journal of neuroscience methods · 2012Article
- Methamphetamine produces bidirectional, concentration-dependent effects on dopamine neuron excitability and dopamine-mediated synaptic currents.Journal of neurophysiology · 2012Article
- Methamphetamine self-administration acutely decreases monoaminergic transporter function.Synapse (New York, N.Y.) · 2012Article
- Biphasic dopamine regulation in mesoaccumbens pathway in response to non-contingent binge and escalating methamphetamine regimens in the Wistar rat.Psychopharmacology · 2011Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
This report demonstrates that a repeated 'challenge' high-dose methamphetamine (METH) injection regimen rapidly decreases striatal K(+)-stimulated dopamine (DA) release concurrent with decreases in both synaptosomal membrane-associated (referred to herein as membrane-associated) and previously reported decreases in non-synaptosomal membrane-associated (presumably cytoplasmic) vesicular DA uptake and content. Resembling previously reported effects involving cytoplasmic vesicles wherein uptake was decreased 48 h after treatment, the decrease in membrane-associated uptake persisted 72 h. Cytoplasmic and membrane-associated vesicular DA uptakes were decreased 7 days after the challenge regimen. A single METH injection also rapidly decreased K(+)-stimulated DA release, membrane-associated DA content, and membrane-associated DA uptake; however, unlike after the challenge regimen, the decrease in uptake recovered by 24 h. Pre-treatment with the D(2) receptor antagonist, eticlopride, did not attenuate the decrease in membrane-associated uptake as assessed 1 h after either a single or challenge treatment. However, eticlopride attenuated the decrease in membrane-associated uptake caused by the challenge regimen as assessed 24 h later. These data reveal complex effects of METH on vesicular function that vary according to the vesicle population under study, dosing regimen, and time after treatment. These may contribute to both the decrease in K(+)-stimulated DA release and the persistent dopaminergic deficits caused by METH.
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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.