Evidence map›Paper›PMID 18477764›Full record

ArticleFASEB journal : official publication of the Federation of American Societies for Experimental Biology2008

Evidence for defective mesolimbic dopamine exocytosis in obesity-prone rats.

Brenda M Geiger, Gerald G Behr, Lauren E Frank, Angela D Caldera-Siu, Margery C Beinfeld, Efi G Kokkotou, Emmanuel N Pothos

Open access · greenAbstract read
In one paragraph

Article in FASEB journal : official publication of the Federation of American Societies for Experimental Biology, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 97 papers.

0numbers the graph read from it
0cells of the map it votes in
97citing papers in PubMed
5.5field-weighted citation impact, top 3% 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

97 citing papers in PubMed, 194 citations in OpenAlex.

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37 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

7 authors at 2 institutions in 2 countries.

Brenda M GeigerDepartment of Pharmacology and Experimental Therapeutics, Tufts University School of Medicine, Boston, Massachusetts 02111, USA.
Gerald G Behr
Lauren E Frank
Angela D Caldera-Siu
Margery C Beinfeld
Efi G Kokkotou
Emmanuel N Pothos
Tufts University · USBeth Israel Deaconess Medical Center · US

Funding

TUSM/T-NEMC CENTER FOR NEUROSCIENCE RESEARCH - Imaging CoreP30NS047243 · NINDS · TUFTS UNIVERSITY BOSTON · PI JACKSON, F ROB · 2003 to 2017
$10.0M
PILOT AND FEASIBILITY STUDIESP30DK034928 · NIDDK · TUFTS MEDICAL CENTER · PI KANE, ANNE VIRGINIA · 1986 to 2007
$8.5M
Effects of dietary obesity on midbrain dopamine systemsR01DK065872 · NIDDK · TUFTS UNIVERSITY BOSTON · PI POTHOS, EMMANUEL N · 2005 to 2009
$1.7M
CNS Dopamine as Marker for Obesity Predisposition: Link to Food and Drug RewardF31DA023760 · NIDA · TUFTS UNIVERSITY BOSTON · PI GEIGER, BRENDA · 2007 to 2010
$142k
NIDA NIH HHS DA023760NIDA NIH HHS F31 DA023760NIDDK NIH HHS DK065872NIDDK NIH HHS P30 DK034928NIDDK NIH HHS P30 DK34928NIDDK NIH HHS R01 DK065872NINDS NIH HHS P30 NS047243
6 · The paper itself

Abstract

The association between dietary obesity and mesolimbic systems that regulate hedonic aspects of feeding is currently unresolved. In the present study, we examined differences in baseline and stimulated central dopamine levels in obesity-prone (OP) and obesity-resistant (OR) rats. OP rats were hyperphagic and showed a 20% weight gain over OR rats at wk 15 of age, when fed a standard chow diet. This phenotype was associated with a 50% reduction in basal extracellular dopamine, as measured by a microdialysis probe in the nucleus accumbens, a projection site of the mesolimbic dopamine system that has been implicated in food reward. Similar defects were also observed in younger animals (4 wk old). In electrophysiology studies, electrically evoked dopamine release in slice preparations was significantly attenuated in OP rats, not only in the nucleus accumbens but also in additional terminal sites of dopamine neurons such as the accumbens shell, dorsal striatum, and medial prefrontal cortex, suggesting that there may be a widespread dysfunction in mechanisms regulating dopamine release in this obesity model. Moreover, dopamine impairment in OP rats was apparent at birth and associated with changes in expression of several factors regulating dopamine synthesis and release: vesicular monoamine transporter-2, tyrosine hydroxylase, dopamine transporter, and dopamine receptor-2 short-form. Taken together, these results suggest that an attenuated central dopamine system would reduce the hedonic response associated with feeding and induce compensatory hyperphagia, leading to obesity.

Indexed as

AnimalsBase SequenceDNA PrimersDopamineElectric StimulationExocytosisFemaleGene ExpressionIn Vitro TechniquesLimbic SystemNeural PathwaysNucleus AccumbensObesityRatsRats, Inbred StrainsRNA, MessengerDNA PrimersDopamineRNA, MessengerSlc18a2 protein, ratTyrosine 3-MonooxygenaseVesicular Monoamine Transport Proteins

Identifiers

PMID18477764
PMCPMC2728544
OpenAlexW2060802299

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.