Evidence map›Paper›PMID 26162812›Full record

ArticleCell calcium2015

Amphetamine activates calcium channels through dopamine transporter-mediated depolarization.

Krasnodara N Cameron, Ernesto Solis, Iwona Ruchala, Louis J De Felice, Jose M Eltit

Open access · greenAbstract read
In one paragraph

Article in Cell calcium, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
1.4field-weighted citation impact, top 23% 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

20 citing papers in PubMed, 34 citations in OpenAlex.

  1. Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. A high-affinity cocaine binding site associated with the brain acid soluble protein 1.Proceedings of the National Academy of Sciences of the United States of America · 2022
    Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
  14. Using CaPsychopharmacology · 2019
    Review
  15. Interactions between Cocaine and the Putative Allosteric Dopamine Transporter Ligand SRI-31142.The Journal of pharmacology and experimental therapeutics · 2018
    Article
  16. Article
  17. Review
  18. N-Alkylated Analogs of 4-Methylamphetamine (4-MA) Differentially Affect Monoamine Transporters and Abuse Liability.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2017
    Article
  19. Article
  20. 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

5 authors at 1 institution in 1 country.

Krasnodara N CameronDepartment of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, United States.
Ernesto SolisDepartment of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, United States.
Iwona RuchalaDepartment of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, United States.
Louis J De FeliceDepartment of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, United States.
Jose M EltitDepartment of Physiology and Biophysics, School of Medicine, Virginia Commonwealth University, Richmond, VA 23298, United States. Electronic address: jmeltit@vcu.edu.
Virginia Commonwealth University · US

Funding

Synthetic cathinones: a new class of illicit drugs affecting DAT & SERTR01DA033930 · NIDA · VIRGINIA COMMONWEALTH UNIVERSITY · PI ELTIT, JOSE MIGUEL, GLENNON, RICHARD A · 2012 to 2016
$2.7M
NIDA NIH HHS R01 DA033930
6 · The paper itself

Abstract

Amphetamine (AMPH) and its more potent enantiomer S(+)AMPH are psychostimulants used therapeutically to treat attention deficit hyperactivity disorder and have significant abuse liability. AMPH is a dopamine transporter (DAT) substrate that inhibits dopamine (DA) uptake and is implicated in DA release. Furthermore, AMPH activates ionic currents through DAT that modify cell excitability presumably by modulating voltage-gated channel activity. Indeed, several studies suggest that monoamine transporter-induced depolarization opens voltage-gated Ca(2+) channels (CaV), which would constitute an additional AMPH mechanism of action. In this study we co-express human DAT (hDAT) with Ca(2+) channels that have decreasing sensitivity to membrane depolarization (CaV1.3, CaV1.2 or CaV2.2). Although S(+)AMPH is more potent than DA in transport-competition assays and inward-current generation, at saturating concentrations both substrates indirectly activate voltage-gated L-type Ca(2+) channels (CaV1.3 and CaV1.2) but not the N-type Ca(2+) channel (CaV2.2). Furthermore, the potency to achieve hDAT-CaV electrical coupling is dominated by the substrate affinity on hDAT, with negligible influence of L-type channel voltage sensitivity. In contrast, the maximal coupling-strength (defined as Ca(2+) signal change per unit hDAT current) is influenced by CaV voltage sensitivity, which is greater in CaV1.3- than in CaV1.2-expressing cells. Moreover, relative to DA, S(+)AMPH showed greater coupling-strength at concentrations that induced relatively small hDAT-mediated currents. Therefore S(+)AMPH is not only more potent than DA at inducing hDAT-mediated L-type Ca(2+) channel currents but is a better depolarizing agent since it produces tighter electrical coupling between hDAT-mediated depolarization and L-type Ca(2+) channel activation.

Indexed as

AmphetamineCalciumCalcium Channel AgonistsCalcium ChannelsDopamine Plasma Membrane Transport ProteinsHEK293 CellsHumansMembrane PotentialsAmphetamineCalciumCalcium Channel AgonistsCalcium ChannelsDopamine Plasma Membrane Transport ProteinsExcitabilityL-type Ca(2+) channelsMDMAMonoamine transportersNeurotransmitter transportSerotoninStimulants

Identifiers

PMID26162812
PMCPMC4631700
OpenAlexW892382653

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.