The DOI matches its Crossref record; 162 of the 166 references it cites were found in a registry or an index.
The Dopamine Transporter and Attention-Deficit/Hyperactivity Disorder
Abstract
The high incidence of attention-deficit/hyperactivity disorder (ADHD) and escalating use of ADHD medications present a compelling case for clarifying the pathophysiology of, and developing laboratory or radiologic tests for, ADHD. Currently, the majority of specific genes implicated in ADHD encode components of catecholamine signaling systems. Of these, the dopamine transporter (DAT) is a principal target of the most widely used antihyperactivity medications (amphetamine and methylphenidate); the DAT gene is associated with ADHD, and some studies have detected abnormal levels of the DAT in brain striatum of ADHD subjects. Medications for ADHD interfere with dopamine transport by brain-region- and drug-specific mechanisms, indirectly activating dopamine- and possibly norepinephrine-receptor subtypes that are implicated in enhancing attention and experiential salience. The most commonly used DAT-selective ADHD medications raise extracellular dopamine levels in DAT-rich brain regions. In brain regions expressing both the DAT and the norepinephrine transporter (NET), the relative contributions of dopamine and norepinephrine to ADHD pathophysiology and therapeutic response are obfuscated by the capacity of the NET to clear dopamine as well as norepinephrine. Thus, ADHD medications targeting DAT or NET might disperse dopamine widely and consign dopamine storage and release to regulation by noradrenergic, as well as dopaminergic neurons.
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“Levels of tonic and phasic DA have also been found to be lower in individuals with ADHD [453,496] whereas the density of DATs, which downregulate DA activity, is higher in ADHD [448,449].”
From Reward circuitry dysfunction in psychiatric and neurodevelopmental disorders and genetic syndromes: animal models and clinical findings (2012) · cites this paper as [496]
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Cites
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Dopamine: Functions, Signaling, and Association with Neurological Diseases
Klein, M. O., Battagello, D. S., Cardoso, A. R., Hauser, D. N., Bittencourt, J. C., & Correa, R. G. (2019) · Cellular and Molecular Neurobiology · doi:10.1007/s10571-018-0632-3 · Cited by 1,073
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Metadata
- Authors
- Madras, B. K., Miller, G. M., & Fischman, A. J.
- Affiliations
- Harvard University (US)
- Massachusetts General Hospital (US)
- Corresponding author
- Madras, Bertha K.
- Venue
- Biological Psychiatry
- Publisher
- Elsevier BV
- Published
- 2005-06
- Volume
- 57
- Issue
- 11
- Pages
- 1397-1409
- ISSN
- 0006-3223 (ISSN-L)
- OpenAlex
- W2011083427
- Cited by
- 393
- References
- 166
- Citations by year
- 2026: 10 · 2025: 20 · 2024: 9 · 2023: 13 · 2022: 11 · 2021: 12 · 2020: 18 · 2019: 10 · 2018: 11 · 2017: 11 · 2016: 14 · 2015: 15 · 2014: 23 · 2013: 16 · 2012: 27
- FWCI
- 4.54
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Biological Psychiatry (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institute on Drug Abuse (DA 06303, R01DA011558, K05DA015305, DA15305, DA 11558)
- National Center for Research Resources (RR00 168)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Psychiatry and Mental health › Schizophrenia research and treatment
- Keywords
- dopamine transporter, attention deficit hyperactivity disorder, ADHD pathophysiology, catecholamine signaling, norepinephrine transporter, amphetamine, methylphenidate, striatum, dopamine, norepinephrine, ADHD medication, genetic susceptibility
- MeSH terms
- Adaptation, Physiological, Central Nervous System Stimulants, Animals, Attention Deficit Disorder with Hyperactivity, Diagnostic Imaging, Humans, Membrane Glycoproteins, Mutation, Nerve Tissue Proteins, Genetic Variation, Membrane Transport Proteins, Dopamine Plasma Membrane Transport Proteins, Vesicular Biogenic Amine Transport Proteins
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