Evidence map›Paper›PMID 21519339›Full record

ReviewMolecular psychiatry2011

New medications for drug addiction hiding in glutamatergic neuroplasticity.

P W Kalivas, N D Volkow

Open access · bronzeAbstract readReview
In one paragraph

Review in Molecular psychiatry, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 207 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
207citing papers in PubMed, 2 pooled it
11.4field-weighted citation impact, top 1% 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

207 citing papers in PubMed, 2 syntheses or guidelines pooled it, 349 citations in OpenAlex.

  1. Pooled it
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  3. A Randomized Controlled Trial of N-acetylcysteine for Adolescent and Young Adult Alcohol Use Disorder.Journal of the American Academy of Child and Adolescent Psychiatry · 2026
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  5. The neural and psychophysiological effects of cannabidiol in youth with alcohol use disorder: A randomized controlled clinical trial.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025
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  16. A randomized, double-blind, placebo-controlled, trial of lamotrigine therapy in bipolar disorder, depressed or mixed phase and cocaine dependence.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2012
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  18. Article
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147 more citing papers are in PubMed but not listed here.

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 2 institutions in 1 country.

P W KalivasDepartment of Neurosciences, Medical University of South Carolina, Charleston National Institute on Drug Abuse, Charleston, SC 29425, USA. kalivasp@musc.edu
N D Volkow
Medical University of South Carolina · USNational Institute on Drug Abuse · US

Funding

Neurobiology of Substance Abuse and AddictionZIAAA000550 · NIAAA · NATIONAL INSTITUTE ON ALCOHOL ABUSE AND ALCOHOLISM · PI VOLKOW, NORA D. · 2009 to 2025
$115.1M
Intramural NIH HHS Z99 DA999999
6 · The paper itself

Abstract

The repeated use of drugs that directly or indirectly stimulate dopamine transmission carry addiction liability and produce enduring pathological changes in the brain circuitry that normally regulates adaptive behavioral responding to a changing environment. This circuitry is rich in glutamatergic projections, and addiction-related behaviors in animal models have been linked to impairments in excitatory synaptic plasticity. Among the best-characterized glutamatergic projection in this circuit is the prefrontal efferent to the nucleus accumbens. A variety of molecular adaptations have been identified in the prefrontal glutamate synapses in the accumbens, many of which are induced by different classes of addictive drugs. Based largely on work with cocaine, we hypothesize that the drug-induced adaptations impair synaptic plasticity in the cortico-accumbens projection, and thereby dysregulate the ability of addicts to control their drug-taking habits. Accordingly, we go on to describe the literature implicating the drug-induced changes in protein content or function that impinge upon synaptic plasticity and have been targeted in preclinical models of relapse and, in some cases, in pilot clinical trials. Based upon modeling drug-induced impairments in neuroplasticity in the cortico-accumbens pathway, we argue for a concerted effort to clinically evaluate the hypothesis that targeting glial and neuronal proteins regulating excitatory synaptic plasticity may prove beneficial in treating addiction.

Indexed as

Adaptation, PhysiologicalBehavior, AddictiveExcitatory Amino Acid AgentsGlutamic AcidHumansNeural PathwaysNeuronal PlasticityNucleus AccumbensPrefrontal CortexSubstance-Related DisordersExcitatory Amino Acid AgentsGlutamic Acid

Identifiers

PMID21519339
PMCPMC3192324
OpenAlexW2019860362

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.