Evidence map›Paper›PMID 23623751›Full record

ArticleBiochemical pharmacology2013

Adolescence methylphenidate treatment in a rodent model of attention deficit/hyperactivity disorder: dopamine transporter function and cellular distribution in adulthood.

Sucharita S Somkuwar, Mahesh Darna, Kathleen M Kantak, Linda P Dwoskin

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.

0numbers the graph read from it
0cells of the map it votes in
25citing papers in PubMed
3.6field-weighted citation impact, top 7% 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

25 citing papers in PubMed, 36 citations in OpenAlex.

  1. Effects of Methylphenidate on the Dopamine Transporter and Beyond.Current topics in behavioral neurosciences · 2022
    Article
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  4. Review
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  16. Differential Pharmacological Regulation of Sensorimotor Gating Deficit in CB1 Knockout Mice and Associated Neurochemical and Histological Alterations.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2015
    Article
  17. Article
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  20. Neuron membrane trafficking and protein kinases involved in autism and ADHD.International journal of molecular sciences · 2015
    Review
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, 789 South Limestone, University of Kentucky, Lexington, KY 40536, USA.
Mahesh Darna
Kathleen M Kantak
Linda P Dwoskin
University of Kentucky · USBoston University · 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 DA011716NIDA NIH HHS R01DA011716
6 · The paper itself

Abstract

Attention deficit/hyperactivity disorder (ADHD) is attributed to dysfunction of the prefrontal cortex. Methylphenidate, an inhibitor of dopamine and norepinephrine transporters (DAT and NET, respectively), is a standard treatment for ADHD. The Spontaneously Hypertensive Rat (SHR) is a well-established animal model of ADHD. Our previous results showed that methylphenidate treatment in adolescent SHR enhanced cocaine self-administration during adulthood, and alterations in DAT function in prefrontal cortex play a role in this response. Importantly, prefrontal cortex subregions, orbitofrontal cortex (OFC) and medial prefrontal cortex (mPFC), have been shown to have distinct roles in ADHD and cocaine self-administration. In the current study, SHR, Wistar-Kyoto (WKY) and Wistar (WIS) rats received a therapeutically relevant dose of methylphenidate (1.5mg/kg, p.o.) or vehicle during adolescence and then OFC and mPFC DAT function and cellular expression were assessed during adulthood. In both OFC and mPFC, no strain differences in Vmax or Km for dopamine uptake into synaptosomes were found between vehicle-treated SHR, WKY and WIS. Methylphenidate increased DAT Vmax in SHR mPFC and decreased DAT Vmax in WKY OFC. Also, methylphenidate decreased DAT Km in WIS OFC. Further, methylphenidate did not alter DAT cellular localization, indicating that methylphenidate treatment during adolescence regulated DAT function in SHR mPFC in a trafficking-independent manner. Thus, the increase in mPFC DAT function was an SHR-specific long term consequence of methylphenidate treatment during adolescence, which may be responsible for the treatment-induced alterations in behavior including the observed increases in cocaine self-administration.

Indexed as

Disease Models, AnimalAnimalsAttention Deficit Disorder with HyperactivityCentral Nervous System StimulantsDopamine Plasma Membrane Transport ProteinsMaleMethylphenidateRatsRats, Inbred SHRRats, Inbred WKYCentral Nervous System StimulantsDopamine Plasma Membrane Transport ProteinsMethylphenidate

Identifiers

PMID23623751
PMCPMC3709249
OpenAlexW2077398583

What OpenQuestion holds

Textmetadata
LicenceTDM
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.