Evidence map›Paper›PMID 20570248›Full record

ArticleBiological psychiatry2010

Peroxisome proliferator-activated receptors-alpha modulate dopamine cell activity through nicotinic receptors.

Miriam Melis, Stefano Carta, Liana Fattore, Stefania Tolu, Sevil Yasar, Steven R Goldberg, Walter Fratta, Uwe Maskos, Marco Pistis

Open access · greenAbstract read
In one paragraph

Article in Biological psychiatry, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 49 papers.

0numbers the graph read from it
0cells of the map it votes in
49citing papers in PubMed
5.9field-weighted citation impact, top 4% 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

49 citing papers in PubMed, 87 citations in OpenAlex.

  1. Initial Evaluation of Fenofibrate for Efficacy in Aiding Smoking Abstinence.Nicotine & tobacco research : official journal of the Society for Research on Nicotine and Tobacco · 2016
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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

9 authors at 6 institutions in 3 countries.

Miriam MelisB.B. Brodie Department of Neuroscience, University of Cagliari, Monserrato, Italy. myriam@unica.it
Stefano Carta
Liana Fattore
Stefania Tolu
Sevil Yasar
Steven R Goldberg
Walter Fratta
Uwe Maskos
Marco Pistis
University of Cagliari · ITInstitut Pasteur · FRJohns Hopkins Medicine · USNational Institutes of Health · USNational Research Council · ITNeuroscience Institute · IT

Funding

Control Of Behavior By Drug InjectionsZIADA000001 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI SHAHAM, YAVIN · 2009 to 2016
$8.3M
Drugs On Learned & Spontaneous Behavior Of Experimental AnimalsZIADA000003 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI SHAHAM, YAVIN · 2009 to 2017
$6.8M
CONTROL OF BEHAVIOR BY DRUG INJECTIONZ01DA000001 · NIDA · NATIONAL INSTITUTE ON DRUG ABUSE · PI GOLDBERG, STEVEN R · 1991 to 2008
$2.8M
Intramural NIH HHS Z01 DA000001
6 · The paper itself

Abstract

backgroundModulation of midbrain dopamine neurons by nicotinic acetylcholine receptors (nAChRs) plays an important role in behavior, cognition, motivation, and reward. Specifically, nAChRs containing beta2 subunits (beta2-nAChRs) switch dopamine cells from a resting to an excited state. However, how beta2-nAChRs can be modulated and thereby how dopamine firing activity is affected remains elusive. Because changes in dopamine cell activity are reflected in the dynamics of microcircuits generating altered responses to stimuli and inputs, factors regulating their state are fundamental. Among these, endogenous ligands to the nuclear receptor-transcription factor peroxisome proliferator-activated receptors type-alpha (PPARalpha) have been recently found to suppress nicotine-induced responses of dopamine neurons.

methodsWe used both in vitro and in vivo electrophysiological techniques together with behavioral analysis to investigate on the effects of modulation of PPARalpha in Sprague-Dawley rat and C57BLJ/6 mouse dopamine neurons and their interactions with beta2-nAChRs. To this aim, we took advantage of a selective reexpression of beta2-nAChR exclusively in dopamine cells by stereotaxically injecting a lentiviral vector in the mouse ventral tegmental area.

resultsWe found that activation of PPARalpha decreases in vitro both dopamine cell activity and ventral tegmental area net output through negative modulation of beta2-nAChRs. Additionally, PPARalpha activation in vivo reduces both the number of spontaneously active dopamine neurons and nicotine-induced increased locomotion.

conclusionsOur combined findings suggest PPARalpha ligands as important negative modulators of beta2-nAChRs on dopamine neurons. Thus, PPARalpha ligands might prove beneficial in treating disorders in which dopamine dysfunction plays a prominent role, such as schizophrenia and nicotine addiction.

Indexed as

Analysis of VarianceAnimalsDopamineMaleMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMotor ActivityNeuronsPPAR alphaRatsRats, Sprague-DawleyReceptor Cross-TalkReceptors, NicotinicSignal TransductionDopaminePPAR alphaReceptors, Nicotinic

Identifiers

PMID20570248
PMCPMC2907468
OpenAlexW2021982247

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.