Evidence map›Paper›PMID 17868653›Full record

ArticleBiochemical pharmacology2007

Bupropion inhibits the cellular effects of nicotine in the ventral tegmental area.

Huibert D Mansvelder, Zara M Fagen, Ben Chang, Robert Mitchum, Daniel S McGehee

Open access · greenAbstract read
In one paragraph

Article in Biochemical pharmacology, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
1.3field-weighted citation impact, top 20% 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

15 citing papers in PubMed, 35 citations in OpenAlex.

  1. Trial
  2. Trial
  3. Bupropion response on sleep quality in patients with depression: implications for increased cardiovascular disease risk.European neuropsychopharmacology : the journal of the European College of Neuropsychopharmacology · 2014
    Trial
  4. Trial
  5. Review
  6. Immediate and Sustained Decrease in Smoking Urges After Acute Insular Cortex Damage.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2017
    Observational
  7. Article
  8. Article
  9. The dynamics of DNA methylation in schizophrenia and related psychiatric disorders.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2013
    Review
  10. Article
  11. Article
  12. Article
  13. Review
  14. Article
  15. 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.

Huibert D MansvelderDepartment of Anesthesia & Critical Care, University of Chicago, Chicago, IL 60637, USA.
Zara M Fagen
Ben Chang
Robert Mitchum
Daniel S McGehee
University of Chicago · US

Funding

NEUROPSYCHOPHARMACOLOLGY TRG FOR DRUG ABUSE RESEARCHT32DA007255 · NIDA · UNIVERSITY OF CHICAGO · PI VEZINA, PAUL R · 1991 to 2012
$5.9M
THE UPREGULATION OF NICOTINIC RECEPTORSP01DA019695 · NIDA · UNIVERSITY OF CHICAGO · PI VEZINA, PAUL R · 2007 to 2011
$4.5M
Nicotinic Modulation of the Mesoaccumbens Dopamine SystemR01DA015918 · NIDA · UNIVERSITY OF CHICAGO · PI MCGEHEE, DANIEL S · 2003 to 2007
$1.9M
REGULATION OF TRANSMISSION BY PRESYNAPTIC RECEPTORSR01NS035090 · NINDS · UNIVERSITY OF CHICAGO · PI MCGEHEE, DANIEL S · 1997 to 1999
–
NIDA NIH HHS DA015918NIDA NIH HHS DA019695NIDA NIH HHS DA07255NIDA NIH HHS P01 DA019695NIDA NIH HHS R01 DA015918NIDA NIH HHS T32 DA007255NINDS NIH HHS R01 NS035090
6 · The paper itself

Abstract

Each year, tobacco use causes over 4 million deaths worldwide and billions of dollars are spent on treatment for tobacco-related illness. Bupropion, an atypical antidepressant, improves the rates of successful smoking cessation, however, the mechanisms by which bupropion reduces cigarette smoking and depression are unknown. Here we show that clinical concentrations of bupropion inhibit nicotine's stimulatory effects on brain reward areas. Many drugs of abuse, including nicotine, stimulate dopamine (DA) release in the mesoaccumbens reward system. Nicotinic acetylcholine receptors in the ventral tegmental area (VTA) mediate nicotine's stimulation of DA release, as well as its rewarding effects. Nicotinic receptors are expressed by excitatory and inhibitory neurons that control DA neuron excitability, and by the DA neurons themselves. Bupropion is a broad-spectrum non-competitive nicotinic receptor antagonist. Here we report that pre-treatment of brain slices with a clinically relevant concentration of bupropion dramatically reduces the effects of nicotine on DA neuron excitability. Nicotinic receptors on VTA DA neurons and their synaptic inputs are inhibited by 75 - 95% after bupropion treatment. We also find that bupropion alone reduces GABAergic transmission to DA neurons, thereby diminishing tonic inhibition of these neurons. This increases DA neuron excitability during bupropion treatment in the absence of nicotine, and may contribute to bupropion's antidepressant actions.

Indexed as

Action PotentialsAnimalsBupropiongamma-Aminobutyric AcidGlutamic AcidNicotinic AntagonistsRatsRats, Sprague-DawleySynaptic TransmissionVentral Tegmental AreaBupropiongamma-Aminobutyric AcidGlutamic AcidNicotinic Antagonists

Identifiers

PMID17868653
PMCPMC2067251
OpenAlexW2166474465

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.