Evidence map›Paper›PMID 18035407›Full record

ReviewPharmacology, biochemistry, and behavior2008

Actions of 3,4-methylenedioxymethamphetamine (MDMA) on cerebral dopaminergic, serotonergic and cholinergic neurons.

Gary A Gudelsky, Bryan K Yamamoto

Abstract readReview
In one paragraph

Review in Pharmacology, biochemistry, and behavior, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 papers.

0numbers the graph read from it
0cells of the map it votes in
53citing papers in PubMed
14.5field-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

53 citing papers in PubMed, 140 citations in OpenAlex.

  1. Trial
  2. Trial
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  4. 5-HTMolecular psychiatry · 2025
    Article
  5. Review
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  7. Article
  8. Article
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  11. Review
  12. Hallucinogens in Mental Health: Preclinical and Clinical Studies on LSD, Psilocybin, MDMA, and Ketamine.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021
    Review
  13. Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
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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 2 institutions in 1 country.

Gary A GudelskyUniversity of Cincinnati, James L. Winkle College of Pharmacy, 3225 Eden Ave., Cincinnati, OH 45267, United States. Gary.Gudelsky@uc.edu
Bryan K Yamamoto
Boston University · USUniversity of Cincinnati Medical Center · US

Funding

METHAMPHETAMINE TOXICITY AND CORTICOSTRIATAL GLUTAMATER01DA007606 · NIDA · UNIVERSITY OF TOLEDO HEALTH SCI CAMPUS · PI YAMAMOTO, BRYAN K · 1992 to 2016
$5.1M
MICRODIALYSIS STUDIES ON MDMA-INDUCED NEUROTOXICITYR01DA007427 · NIDA · UNIVERSITY OF CINCINNATI · PI GUDELSKY, GARY · 1992 to 2010
$2.8M
Chronic Stress and MDMA NeurotoxicityR01DA016866 · NIDA · BOSTON UNIVERSITY MEDICAL CAMPUS · PI YAMAMOTO, BRYAN K · 2003 to 2006
$1.3M
NIDA NIH HHS DA07427NIDA NIH HHS DA07606NIDA NIH HHS DA16866NIDA NIH HHS R01 DA007427NIDA NIH HHS R01 DA007606NIDA NIH HHS R01 DA016866
6 · The paper itself

Abstract

3,4-Methylenedioxymethamphetamine (MDMA) is an amphetamine derivative and a popular drug of abuse that exhibits mild hallucinogenic and rewarding properties and engenders feelings of connectedness and openness. The unique psychopharmacological profile of this drug of abuse most likely is derived from the property of MDMA to promote the release of dopamine and serotonin (5-HT) in multiple brain regions. The present review highlights primarily data from studies employing in vivo microdialysis that detail the actions of MDMA on the release of these neurotransmitters. Data from in vivo microdialysis experiments indicate that MDMA, like most amphetamine derivatives, increases the release of dopamine in the striatum, n. accumbens and prefrontal cortex. However, the release of dopamine evoked by MDMA in each of these brain regions appears to be modulated by concomitantly released 5-HT and the subsequent activation of 5-HT2A/C or 5-HT2B/C receptors. In addition to its stimulatory effect on the release of monoamines, MDMA also enhances the release of acetylcholine in the striatum, hippocampus and prefrontal cortex, and this cholinergic response appears to be secondary to the activation of histaminergic, dopaminergic and/or serotonergic receptors. Beyond the acute stimulatory effect of MDMA on neurotransmitter release, MDMA also increases the extracellular concentration of energy substrates, e.g., glucose and lactate in the brain. In contrast to the acute stimulatory actions of MDMA on the release of monoamines and acetylcholine, the repeated administration of high doses of MDMA is thought to result in a selective neurotoxicity to 5-HT axon terminals in the rat. Additional studies are reviewed that focus on the alterations in neurotransmitter responses to pharmacological and physiological stimuli that accompany MDMA-induced 5-HT neurotoxicity.

Indexed as

MicrodialysisAcetylcholineAnimalsBrainCorpus StriatumDopamineGlucoseHippocampusHumansN-Methyl-3,4-methylenedioxyamphetamineNucleus AccumbensPrefrontal CortexSerotoninAcetylcholineDopamineGlucoseN-Methyl-3,4-methylenedioxyamphetamineSerotonin

Identifiers

PMID18035407
PMCPMC2505334
OpenAlexW2015485611

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.