Therapeutic doses of amphetamine and methylphenidate selectively redistribute the vesicular monoamine transporter-2
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High-dose administration of psychostimulants traffics the vesicular monoamine transporter-2 (VMAT-2), as assessed by subcellular fractionation of rat striatal tissue. This study demonstrates that administration of low doses of amphetamine or methylphenidate differentially traffic VMAT-2 within nerve terminals, with effects similar to those observed after high-dose administration. Trafficking of vesicular glutamate, acetylcholine, or GABA transporters was not altered by high-or low-dose amphetamine or methylphenidate treatment. These data represent the first report that amphetamine redistributes VMAT-2 protein. In addition, these data demonstrate that the trafficking of VMAT-2 after amphetamine or methylphenidate is selective for monoaminergic neurons.
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Amphetamine also inhibits VMAT-2, increasing vesicular dopamine release and causing reverse transport of cytosolic dopamine via DAT.
“AMP also increases vesicular DA release via inhibition of the vesicular monoamine transporter 2 (VMAT-2), which releases DA from vesicular storage, and the concomitant release of cytosolic DA via reverse transport by the DAT (58, 88, 99).”
The increase of DA promotes dopaminergic transmission by regulating (inhibiting) VMAT2, SERT (with weaker affinity), and MAOA and MAOB.
“The increase of DA promotes the dopaminergic transmission by regulating (inhibiting) other proteins: VMAT2, whose inhibition induces the DA liberation from vesicular storage and the concomitant release of cytosolic DA via DAT reverse transport [33, 187], SERT (with weaker affinity), and MAOA and MAOB [153].”
From Molecular Characterisation of the Mechanism of Action of Stimulant Drugs Lisdexamfetamine and Methylphenidate on ADHD Neurobiology: A Review (2022) · cites this paper as [187]
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Faraone, S. V. (2018) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2018.02.001 · Cited by 631 · see citing works
The neuropharmacology of ADHD drugs in vivo: Insights on efficacy and safety
Heal, D. J., Cheetham, S. C., & Smith, S. L. (2009) · Neuropharmacology · doi:10.1016/j.neuropharm.2009.08.020 · Cited by 198 · see citing works
Illicit dopamine transients: reconciling actions of abused drugs
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“ergic transmission by regulating (inhibiting) other proteins: VMAT2, whose inhibition induces the DA liberation from vesicular storage and the concomitant release of cytosolic DA via DAT reverse transport [33, 187], SERT (with weaker affinity), and MAOA and MAOB [153].”
BackgroundLuikinga, S. J., Kim, J. H., & Perry, C. J. (2018) · Progress in Neuro-Psychopharmacology and Biological Psychiatry · doi:10.1016/j.pnpbp.2017.11.010 · Cited by 59 · see citing works
- Authors
- Riddle, E. L., Hanson, G. R., & Fleckenstein, A. E.
- Affiliations
- University of Utah (US)
- Corresponding author
- Riddle, Evan L.
- Venue
- European Journal of Pharmacology
- Publisher
- Elsevier BV
- Published
- 2007-09
- Volume
- 571
- Issue
- 1
- Pages
- 25-28
- ISSN
- 0014-2999 (ISSN-L)
- PMC
- PMC2581712
- OpenAlex
- W2001782638
- Cited by
- 49
- References
- 1
- Citations by year
- 2025: 5 · 2024: 5 · 2023: 3 · 2022: 2 · 2021: 4 · 2020: 2 · 2019: 3 · 2018: 2 · 2017: 2 · 2016: 1 · 2014: 4 · 2013: 3 · 2012: 2
- FWCI
- 1.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- European Journal of Pharmacology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Institute on Drug Abuse (R01DA000869, DA 00869, DA 04222, DA 11389, R01DA011389, K05DA000378, P01DA013367, K02DA019447, DA-13367, R29DA011389, R01DA004222)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Cellular transport and secretion
- Keywords
- amphetamine, methylphenidate, vesicular monoamine transporter 2, psychostimulants, striatum, presynaptic terminals, monoaminergic neurons, vesicular glutamate transporter, vesicular acetylcholine transporter, vesicular GABA transporter, subcellular protein distribution
- MeSH terms
- Amphetamine, Central Nervous System Stimulants, Animals, Cell Membrane, Cytoplasm, Dose-Response Relationship, Drug, Immunohistochemistry, Male, Methylphenidate, Synaptosomes, Blotting, Western, Rats, Sprague-Dawley, Protein Transport, Vesicular Monoamine Transport Proteins, Rats
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