Differential Involvement of Dopamine D1And D2Receptors and Inhibition by Dopamine of Hypothalamic VMN Neurons in Early Postnatally Overfed Juvenile Rats
Abstract
Dopamine is among the neurotransmitters involved in central regulation of food intake, and body weight control. To study possible changes in neuronal responses to dopamine, single unit activity of the ventromedial hypothalamic nucleus (VMN) was recorded in brain slices of normal and obese rats. The latter had developed overweight throughout juvenile life (p < 0.05) by early postnatal over-nourishment due to a reduction of litter size from 3rd to 21st day of life (small litters, SL). With effective concentrations of about 100-500 nM/I dopamine inhibited significantly more VMN neurons in obese than normal rats (Chi-square p < 0.05). While D2 receptors in the VMN are reported to mediate inhibition of food intake, the responses to dopamine were blocked by D2 receptor antagonists in significantly fewer neurons of SL than normal rats (p < 0.05). Furthemore, including results of action of D1 receptor agonists we found that significantly more neurons in SL than NL rats seem to express D1 receptors. Thus, increased suppression by dopamine of firing of VMN neurons that signal satiety with a rise in the discharge rate, and changed expression or activity of dopamine receptors might contribute to increased feeding behavior in juvenile rats hyperphagic and overweight due to early postnatal overfeeding.
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Besides classical genetic, epigenetic and nongenetic mechanisms could also be potentially responsible for differences in neural reward circuitry and reward behaviors at a young age, predisposing to hyperphagia and obesity later in life.
“Besides classical genetic, epigenetic and nongenetic mechanisms ([23](#B23), [34](#B34), [36](#B36), [37](#B37), [62](#B62), [67](#B67), [126](#B126), [155](#B155), [176](#B176), [184](#B184)) could also be potentially responsible for differences in neural reward circuitry and reward behaviors at a young age, predisposing to hyperphagia and obesity later in life.”
From Food reward, hyperphagia, and obesity (2011) · cites this paper as [36]
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Bakhshi-Ameshi, S., Torabi, N., Nazari, M., & Eliassi, A. (2025) · Brain Research · doi:10.1016/j.brainres.2025.149846
- Authors
- Davidowa, H., Heidel, E., & Plagemann, A.
- Affiliations
- Humboldt-Universität zu Berlin (DE)
- Corresponding author
- Davidowa, Helga
- ORCID
- Plagemann, Andreas
- Venue
- Nutritional Neuroscience
- Publisher
- Informa UK Limited
- Published
- 2002-01
- Volume
- 5
- Issue
- 1
- Pages
- 27-36
- ISSN
- 1028-415X (ISSN-L)
- 1476-8305
- OpenAlex
- W2029898368
- Cited by
- 21
- References
- 53
- Citations by year
- 2025: 1 · 2021: 1 · 2018: 2 · 2016: 1 · 2013: 1
- FWCI
- 0.53
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Nutritional Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Endocrine and Autonomic Systems › Regulation of Appetite and Obesity
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Reproductive Medicine › Hypothalamic control of reproductive hormones
- Keywords
- dopamine D1 receptor, dopamine D2 receptor, ventromedial hypothalamus, hypothalamic neurons, postnatal overnutrition, youth obesity, dopamine D2 receptor antagonists, D1 receptor agonists, satiety signals, feeding behavior, hyperphagia, single-unit activity
- MeSH terms
- Animals, Dopamine, Female, Hypothalamus, Middle, Male, Neurons, Obesity, Weight Gain, Rats, Wistar, Receptors, Dopamine D1, Receptors, Dopamine D2, Dopamine Agonists, Dopamine Antagonists, Rats, Dopamine D2 Receptor Antagonists
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