Evidence map›Paper›PMID 23822950›Full record

ArticleNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology2013

Adolescent atomoxetine treatment in a rodent model of ADHD: effects on cocaine self-administration and dopamine transporters in frontostriatal regions.

Sucharita S Somkuwar, Chloe J Jordan, Kathleen M Kantak, Linda P Dwoskin

Open access · bronzeAbstract read
In one paragraph

Article in Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed, 1 pooled it
2.7field-weighted citation impact, top 11% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 1 synthesis or guideline pooled it, 39 citations in OpenAlex.

  1. Pooled it
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  11. Sigma-1 Receptor Antagonist (BD1047) Decreases Cathepsin B Secretion in HIV-Infected Macrophages Exposed to Cocaine.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2019
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  14. [Effect of glucocorticoid receptor function on the behavior of rats with attention deficit hyperactivity disorder].Zhongguo dang dai er ke za zhi = Chinese journal of contemporary pediatrics · 2018
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

4 authors at 2 institutions in 1 country.

Sucharita S SomkuwarDepartment of Pharmaceutical Sciences, College of Pharmacy, University of Kentucky, Lexington, KY, USA.
Chloe J Jordan
Kathleen M Kantak
Linda P Dwoskin
Boston University · USUniversity of Kentucky · US

Funding

COGNITIVE ASPECTS OF ADDICTION-RELATED BEHAVIORR01DA011716 · NIDA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI KANTAK, KATHLEEN M. · 1998 to 2013
$4.8M
NIDA NIH HHS R01 DA011716
6 · The paper itself

Abstract

Cocaine abuse and attention deficit/hyperactivity disorder (ADHD) are often comorbid. Preclinical research indicates that medial prefrontal (mPFC) and orbitofrontal (OFC) cortices are important neural substrates for both disorders. Using the spontaneously hypertensive rat (SHR) model of ADHD, we reported that adolescent treatment with the stimulant methylphenidate, a dopamine (DAT) and norepinephrine (NET) transporter inhibitor, enhanced cocaine self-administration during adulthood, and was associated with increased DAT function in mPFC. This study investigates the effects of atomoxetine ((R)-N-methyl-γ-(2-methylphenoxy)-benzenepropanamine hydrochloride) treatment, a selective NET inhibitor, during adolescence on cocaine self-administration and on DAT function and cell-surface expression in mPFC and OFC during adulthood. SHR acquired cocaine self-administration faster than Wistar-Kyoto and Wistar. Across cocaine doses, SHR earned more cocaine infusions and had higher progressive-ratio breakpoints than Wistar-Kyoto and Wistar, demonstrating that the SHR phenotype models comorbid ADHD and cocaine abuse. Prior atomoxetine treatment did not augment cocaine self-administration in SHR, but acquisition was enhanced in Wistar-Kyoto. No strain differences were found for DAT kinetic parameters or cellular localization in the vehicle controls. Atomoxetine did not alter DAT kinetic parameters or localization in SHR mPFC. Rather, atomoxetine decreased V(max) and DAT cell surface expression in SHR OFC, indicating that inhibition of NET by atomoxetine treatment during adolescence indirectly reduced DAT function and trafficking to the cell surface in OFC, specifically in the ADHD model. Thus, atomoxetine, unlike methylphenidate, does not enhance vulnerability to cocaine abuse in SHR and may represent an important alternative for teens with ADHD when drug addiction is a concern.

Indexed as

Adrenergic Uptake InhibitorsAnimalsAtomoxetine HydrochlorideAttention Deficit Disorder with HyperactivityCocaineCorpus StriatumDisease Models, AnimalDopamineDopamine Plasma Membrane Transport ProteinsDopamine Uptake InhibitorsDose-Response Relationship, DrugFrontal LobeMalePropylaminesRatsRats, Inbred SHRAdrenergic Uptake InhibitorsAtomoxetine HydrochlorideCocaineDopamineDopamine Plasma Membrane Transport ProteinsDopamine Uptake InhibitorsPropylamines

Identifiers

PMID23822950
PMCPMC3828528
OpenAlexW2003201642

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.