ArticleeNeuro
VMAT2-Mediated Neurotransmission from Midbrain Leptin Receptor Neurons in Feeding Regulation.
Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Nutritionally Responsive PMv DAT Neurons Are Dynamically Regulated During Pubertal Transition.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Nutritionally responsive PMv DAT neurons are dynamically regulated during pubertal transition.bioRxiv : the preprint server for biology · 2025Article
- Experimental biology can inform our understanding of food insecurity.The Journal of experimental biology · 2024Article
- Lateral septum as a melanocortin downstream site in obesity development.Cell reports · 2023Article
- The regulatory role of AP-2β in monoaminergic neurotransmitter systems: insights on its signalling pathway, linked disorders and theragnostic potential.Cell & bioscience · 2022Review
- Obesity: an evolutionary context.Life metabolism · 2022Review
- Metabotropic glutamate receptor 5 knockout rescues obesity phenotype in a mouse model of Huntington's disease.Scientific reports · 2022Article
- Selective Knockout of theFrontiers in behavioral neuroscience · 2020Article
- Critical Roles of Glutaredoxin in Brain Cells-Implications for Parkinson's Disease.Antioxidants & redox signaling · 2019Review
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Authors and funding
8 authors at 3 institutions in 2 countries.
Funding
Abstract
Leptin receptors (LepRs) expressed in the midbrain contribute to the action of leptin on feeding regulation. The midbrain neurons release a variety of neurotransmitters including dopamine (DA), glutamate and GABA. However, which neurotransmitter mediates midbrain leptin action on feeding remains unclear. Here, we showed that midbrain LepR neurons overlap with a subset of dopaminergic, GABAergic and glutamatergic neurons. Specific removal of vesicular monoamine transporter 2 (VMAT2) in midbrain LepR neurons (KO mice) disrupted DA accumulation in vesicles, but failed to cause a significant change in the evoked release of either glutamate or GABA to downstream neurons. While KO mice showed no differences on chow, they presented a reduced high-fat diet (HFD) intake and resisted to HFD-induced obesity. Specific activation of midbrain LepR neurons promoted VMAT2-dependent feeding on chow and HFD. When tested with an intermittent access to HFD where first 2.5-h HFD eating (binge-like) and 24-h HFD feeding were measured, KO mice exhibited more binge-like, but less 24-h HFD feeding. Interestingly, leptin inhibited 24-h HFD feeding in controls but not in KO mice. Thus, VMAT2-mediated neurotransmission from midbrain LepR neurons contributes to both binge-like eating and HFD feeding regulation.
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Registered trials
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.