Evidence map›Paper›PMID 28605494›Full record

ReviewThe international journal of neuropsychopharmacology2017

Glutamate Transport: A New Bench to Bedside Mechanism for Treating Drug Abuse.

Sade Spencer, Peter W Kalivas

Open access · goldAbstract readReview
In one paragraph

Review in The international journal of neuropsychopharmacology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
3.1field-weighted citation impact, top 8% 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

46 citing papers in PubMed, 71 citations in OpenAlex.

  1. Trial
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  4. An emerging role for synaptic ZnPharmacology & therapeutics · 2026
    Review
  5. Article
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  7. Article
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  12. New Approaches to Addiction Treatment Based on Learning and Memory.Current topics in behavioral neurosciences · 2025
    Review
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  14. Article
  15. Review
  16. Review
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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

2 authors at 1 institution in 1 country.

Sade SpencerDepartment of Neurosciences, Medical University of South Carolina, Charleston, South Carolina.
Peter W KalivasDepartment of Neurosciences, Medical University of South Carolina, Charleston, South Carolina.
Medical University of South Carolina · US

Funding

Selective Restoration of KCNQ Channel Inhibition in the PFC to Inhibit Cue-InducP50DA015369 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI MCGINTY, JACQUELINE F. · 2003 to 2017
$18.6M
GLUTAMATE AND CRAVING FOR COCAINER01DA012513 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KALIVAS, PETER W · 2000 to 2024
$7.5M
OPIOIDS, AMPHETAMINE &COCAIN IN DRUG ABUSER01DA003906 · NIDA · WASHINGTON STATE UNIVERSITY · PI KALIVAS, PETER W · 1985 to 2019
$3.6M
COCAINE, OPIOIDS AND DRUG ABUSER37DA003906 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI KALIVAS, PETER W · 2000 to 2009
$3.0M
The Role of Dopamine in Modulating Relapse-induced Transient Synaptic PlasticityK99DA041462 · NIDA · MEDICAL UNIVERSITY OF SOUTH CAROLINA · PI SPENCER, SADE MONIQUE · 2016 to 2017
$267k
NIDA NIH HHS K99 DA041462NIDA NIH HHS P50 DA015369NIDA NIH HHS R01 DA003906NIDA NIH HHS R01 DA012513NIDA NIH HHS R37 DA003906
6 · The paper itself

Abstract

Drug addiction has often been described as a "hijacking" of the brain circuits involved in learning and memory. Glutamate is the principal excitatory neurotransmitter in the brain, and its contribution to synaptic plasticity and learning processes is well established in animal models. Likewise, over the past 20 years the addiction field has ascribed a critical role for glutamatergic transmission in the development of addiction. Chronic drug use produces enduring neuroadaptations in corticostriatal projections that are believed to contribute to a maladaptive deficit in inhibitory control over behavior. Much of this research focuses on the role played by ionotropic glutamate receptors directly involved in long-term potentiation and depression or metabotropic receptors indirectly modulating synaptic plasticity. Importantly, the balance between glutamate release and clearance tightly regulates the patterned activation of these glutamate receptors, emphasizing an important role for glutamate transporters in maintaining extracellular glutamate levels. Five excitatory amino acid transporters participate in active glutamate reuptake. Recent evidence suggests that these glutamate transporters can be modulated by chronic drug use at a variety of levels. In this review, we synopsize the evidence and mechanisms associated with drug-induced dysregulation of glutamate transport. We then summarize the preclinical and clinical data suggesting that glutamate transporters offer an effective target for the treatment of drug addiction. In particular, we focus on the role that altered glutamate transporters have in causing drug cues and contexts to develop an intrusive quality that guides maladaptive drug seeking behaviors.

Indexed as

AnimalsGlutamate Plasma Membrane Transport ProteinsHumansSubstance-Related DisordersGlutamate Plasma Membrane Transport Proteinsaddictioncellular redoxglutamate transportersn-acetylcysteinerelapse

Identifiers

PMID28605494
PMCPMC5632313
OpenAlexW2742548778

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC
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.