Atomoxetine Increases Extracellular Levels of Norepinephrine and Dopamine in Prefrontal Cortex of Rat A Potential Mechanism for Efficacy in Attention Deficit/Hyperactivity Disorder
Open accessAbstract
The selective norepinephrine (NE) transporter inhibitor atomoxetine (formerly called tomoxetine or LY139603) has been shown to alleviate symptoms in Attention Deficit/Hyperactivity Disorder (ADHD). We investigated the mechanism of action of atomoxetine in ADHD by evaluating the interaction of atomoxetine with monoamine transporters, the effects on extracellular levels of monoamines, and the expression of the neuronal activity marker Fos in brain regions. Atomoxetine inhibited binding of radioligands to clonal cell lines transfected with human NE, serotonin (5-HT) and dopamine (DA) transporters with dissociation constants (K(i)) values of 5, 77 and 1451 nM, respectively, demonstrating selectivity for NE transporters. In microdialysis studies, atomoxetine increased extracellular (EX) levels of NE in prefrontal cortex (PFC) 3-fold, but did not alter 5-HT(EX) levels. Atomoxetine also increased DA(EX) concentrations in PFC 3-fold, but did not alter DA(EX) in striatum or nucleus accumbens. In contrast, the psychostimulant methylphenidate, which is used in ADHD therapy, increased NE(EX) and DA(EX) equally in PFC, but also increased DA(EX) in the striatum and nucleus accumbens to the same level. The expression of the neuronal activity marker Fos was increased 3.7-fold in PFC by atomoxetine administration, but was not increased in the striatum or nucleus accumbens, consistent with the regional distribution of increased DA(EX). We hypothesize that the atomoxetine-induced increase of catecholamines in PFC, a region involved in attention and memory, mediates the therapeutic effects of atomoxetine in ADHD. In contrast to methylphenidate, atomoxetine did not increase DA in striatum or nucleus accumbens, suggesting it would not have motoric or drug abuse liabilities.
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The precise mechanism by which atomoxetine produces its therapeutic effects in ADHD is unknown, but it is thought to be related to selective inhibition of the pre-synaptic norepinephrine transporter, as determined in ex vivo uptake and neurotransmitter depletion studies.
“The precise mechanism by which atomoxetine produces its therapeutic effects in ADHD is unknown, but it is thought to be related to selective inhibition of the pre-synaptic norepinephrine transporter, as determined in ex vivo uptake and neurotransmitter depletion studies [24].”
From Atomoxetine Effects on Executive Function as Measured by the BRIEF-A in Young Adults with ADHD: A Randomized, Double-Blind, Placebo-Controlled Study (2014) · cites this paper as [24]
Split into 2 atoms — 1 confirmed, 1 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredAtomoxetine blocks the norepinephrine transporter, and as the norepinephrine transporter clears both norepinephrine and dopamine in the PFC, this increases extracellular levels of both catecholamines.
“Like methylphenidate, atomoxetine also blocks the NE transporter (Figure 2E), and as the NE transporter clears both NE and DA in the PFC, this increases extracellular levels of both catecholamines (90).”
From Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks (2011) · cites this paper as [90]
The Discussion (page unavailable) reports that atomoxetine inhibits the NE transporter, that this transporter takes up dopamine in the PFC, and that atomoxetine increases extracellular NE and dopamine there. It presents transporter-mediated dopamine clearance as a proposed explanation, however, and says other interactions may also contribute; the citing sentence states that causal explanation more definitively than the paper does. (LLM, conf=0.82)
Experimental — accuracy not yet measuredBecause the norepinephrine transporter clears both norepinephrine and dopamine in the PFC, atomoxetine increases both dopamine and norepinephrine in the rat PFC.
“However, as the NE transporter clears both NE and DA in the PFC, atomoxetine increases both DA and NE in the rat PFC (Bymaster et al., 2002).”
From Catecholamine influences on prefrontal cortical function: Relevance to treatment of attention deficit/hyperactivity disorder and related disorders (2011) · cites this paper as Bymaster et al., 2002
Atomoxetine increases extracellular availability of both norepinephrine and dopamine in the rat PFC.
“Atomoxetine increases extracellular availability of both NE and DA in the rat PFC (Bymaster et al., 2002).”
From Catecholamine influences on prefrontal cortical function: Relevance to treatment of attention deficit/hyperactivity disorder and related disorders (2011) · cites this paper as Bymaster et al., 2002
Stimulant medications and atomoxetine enhance PFC function by indirectly increasing these catecholamine actions through blockade of norepinephrine and/or dopamine transporters.
“The stimulant medications and atomoxetine appear to enhance PFC function by indirectly increasing these catecholamine actions through blockade of norepinephrine and/or dopamine transporters.”
From Catecholamine Influences on Dorsolateral Prefrontal Cortical Networks (2011) · cites this paper as [90]
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Hepatic Events Associated with Atomoxetine Treatment for??Attention-Deficit??Hyperactivity Disorder
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Spotlight on Atomoxetine in Attention-Deficit Hyperactivity Disorder in Children and Adolescents†
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- Authors
- Bymaster, F.
- Affiliations
- Eli Lilly (United States) (US)
- Corresponding author
- Bymaster, F
- Venue
- Neuropsychopharmacology
- Published
- 2002-11
- Volume
- 27
- Issue
- 5
- Pages
- 699-711
- ISSN
- 0893-133X (ISSN-L)
- OpenAlex
- W2057760214
- Cited by
- 1,123
- References
- 7
- Citations by year
- 2026: 25 · 2025: 31 · 2024: 52 · 2023: 47 · 2022: 35 · 2021: 44 · 2020: 40 · 2019: 41 · 2018: 24 · 2017: 49 · 2016: 65 · 2015: 64 · 2014: 77 · 2013: 57 · 2012: 66
- FWCI
- 22.91
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Neuropsychopharmacology (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Psychiatry and Mental health › Attention Deficit Hyperactivity Disorder
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Keywords
- atomoxetine, attention deficit hyperactivity disorder, norepinephrine transporter, dopamine transporter, serotonin transporter, prefrontal cortex, Fos expression, methylphenidate, monoamine transporters, drug selectivity, striatum, nucleus accumbens, drug abuse liability
- MeSH terms
- Atomoxetine Hydrochloride, Animals, Attention Deficit Disorder with Hyperactivity, Dopamine, Drug Synergism, Humans, Male, Norepinephrine, Propylamines, Rats, Sprague-Dawley, Prefrontal Cortex, Rats
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