Evidence for defective mesolimbic dopamine exocytosis in obesity‐prone rats
Open accessAbstract
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.—Geiger, B. M., Behr, G. G., Frank, L. E., Caldera‐Siu, A. D., Beinfeld, M. C., Kokkotou, E. G., Pothos, E. N. Evidence for defective mesolimbic dopamine exocytosis in obesity‐prone rats. FASEB J. 22, 2740–2746 (2008)
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Decreased striatal D2R-related signalling is likely to reduce sensitivity to other natural rewards, and this deficit in obese individuals may contribute to compensatory overeating.
“since decreased striatal D2R-related signalling is also likely to reduce the sensitivity to other natural rewards, this deficit in obese individuals may also contribute to compensatory overeating (88).”
From Obesity and addiction: Neurobiological overlaps (2013) · cites this paper as [88]
Since decreased D2R-related signaling is also likely to reduce sensitivity to other natural rewards, this deficit in obese individuals might also contribute to compensatory overeating.
“In addition, since decreased D2R-related signaling is also likely to reduce the sensitivity to other natural rewards, this deficit in obese individuals might also contribute to compensatory overeating (Geiger et al 2008).”
From Food and Drug Reward: Overlapping Circuits in Human Obesity and Addiction (2011) · cites this paper as Geiger et al 2008
In selectively bred lines of obesity-prone and obesity-resistant rats, several differences in mesolimbic dopamine signaling have been reported.
“In selectively bred lines of obesity-prone and obesity-resistant rats, several differences in mesolimbic dopamine signaling have been reported ([41](#B41), [65](#B65)), but most of these studies used adult, already obese animals.”
From Food reward, hyperphagia, and obesity (2011) · cites this paper as [65]
In only one preliminary study was a difference in mesolimbic dopamine signaling seen at an early age in obesity-prone and obesity-resistant rats.
“In only one preliminary study was a difference seen at an early age ([65](#B65)), so it is not clear whether differences in reward functions are preexisting and genetically determined or acquired by exposure to palatable food stimuli and/or secondary to the obese state.”
From Food reward, hyperphagia, and obesity (2011) · cites this paper as [65]
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- Authors
- Geiger, B. M., Behr, G. G., Frank, L. E., Caldera-Siu, A. D., Beinfeld, M. C., Kokkotou, E. G., & Pothos, E. N.
- Affiliations
- Tufts University (US)
- Beth Israel Deaconess Medical Center (US)
- Venue
- The FASEB Journal
- Publisher
- Wiley
- Published
- 2008-05-13
- Volume
- 22
- Issue
- 8
- Pages
- 2740-2746
- ISSN
- 0892-6638 (ISSN-L)
- 1530-6860
- PMC
- PMC2728544
- OpenAlex
- W2060802299
- Cited by
- 194
- References
- 40
- Citations by year
- 2026: 1 · 2025: 11 · 2024: 4 · 2023: 2 · 2022: 6 · 2021: 5 · 2020: 8 · 2019: 7 · 2018: 9 · 2017: 8 · 2016: 14 · 2015: 18 · 2014: 15 · 2013: 19 · 2012: 19
- FWCI
- 6.92
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- The FASEB Journal (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Center for Neuroscience Research (P30 NS047243)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Social Sciences › Psychology › Clinical Psychology › Eating Disorders and Behaviors
- Keywords
- obesity-prone rats, mesolimbic dopamine system, nucleus accumbens, hyperphagia, food reward, dopamine release, vesicular monoamine transporter 2, tyrosine hydroxylase, dopamine transporter, dopamine D2 receptor, obesity resistance, hedonic feeding
- MeSH terms
- Animals, Base Sequence, Dopamine, Electric Stimulation, Exocytosis, Female, Limbic System, Neural Pathways, Nucleus Accumbens, Obesity, Rats, Inbred Strains, RNA, Messenger, Tyrosine 3-Monooxygenase, Gene Expression, DNA Primers, Vesicular Monoamine Transport Proteins, Rats, In Vitro Techniques
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