Evidence map›Paper›PMID 21863234›Full record

ArticlePsychopharmacology2012

Disulfiram stimulates dopamine release from noradrenergic terminals and potentiates cocaine-induced dopamine release in the prefrontal cortex.

Paola Devoto, Giovanna Flore, Pierluigi Saba, Roberto Cadeddu, Gian Luigi Gessa

Abstract read
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In one paragraph

Article in Psychopharmacology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.

0numbers the graph read from it
0cells of the map it votes in
24citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

24 citing papers in PubMed, 42 citations in OpenAlex.

  1. Trial
  2. Cocaine facilitates CaMolecular psychiatry · 2026
    Article
  3. Mirtazapine decreased cocaine-inducedFrontiers in psychiatry · 2024
    Article
  4. Review
  5. Article
  6. Article
  7. Article
  8. Review
  9. Article
  10. Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Psychostimulant addiction treatment.Neuropharmacology · 2014
    Review
  17. Article
  18. Article
  19. Article
  20. Article
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.

Paola DevotoDepartment of Neuroscience, University of Cagliari, Monserrato, Italy. pdevoto@unica.it
Giovanna Flore
Pierluigi Saba
Roberto Cadeddu
Gian Luigi Gessa
University of Cagliari · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

rationaleDisulfiram efficacy in treatment of cocaine addiction is attributed to the inhibition of dopamine-β-hydroxylase and reduction in brain noradrenaline (NA)/dopamine (DA) ratio.

objectivesUsing microdialysis, we investigated if disulfiram causes DA release from noradrenergic terminals and modifies cocaine-induced DA release.

resultsDisulfiram reduced extracellular NA in the medial prefrontal (mPF) cortex, occipital cortex, accumbens and caudate nuclei, while it markedly increased DA not only in mPF but also in the occipital cortex, despite its scanty dopaminergic afferences, and modestly increased DA in the accumbens and caudate nuclei, despite their dense dopaminergic innervation. Disulfiram-induced DA accumulation was reversed in both cortices by tetrodotoxin infusion and by systemic administration of the α(2)-adrenoceptor agonist clonidine, but was not modified by the α(2)-adrenoceptor antagonist RS 79948 or the D(2)-like agonist quinpirole. Disulfiram prevented cocaine-induced NA release in the mPF cortex and nucleus accumbens, potentiated cocaine-induced DA release in the mPF cortex but failed to modify cocaine effect in the nucleus accumbens. DA release induced by disulfiram-cocaine combination in the mPF cortex was prevented by clonidine but not by quinpirole.

conclusionsWe suggested that disulfiram, by removing NA-mediated inhibitory control on noradrenergic terminals, causes an unrestrained cocaine-induced DA release from those terminals in the mPF cortex. In the accumbens and caudate nuclei, "allogenic" DA concentration might be clouded by DA originated from dopaminergic terminals. The possible role of "allogenic" DA in disulfiram ability to prevent stress-induced reinstatement of cocaine seeking is discussed.

Indexed as

AnimalsBrainCocaineCocaine-Related DisordersDisulfiramDopamineDopamine beta-HydroxylaseEnzyme InhibitorsMaleMicrodialysisNorepinephrinePrefrontal CortexRatsRats, Sprague-DawleyCocaineDisulfiramDopamineDopamine beta-HydroxylaseEnzyme InhibitorsNorepinephrine

Identifiers

PMID21863234
OpenAlexW2066813264

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.