| First Author | Xu Y | Year | 2017 |
| Journal | eNeuro | Volume | 4 |
| Issue | 3 | PubMed ID | 28560316 |
| Mgi Jnum | J:255950 | Mgi Id | MGI:6114251 |
| Doi | 10.1523/ENEURO.0083-17.2017 | Citation | Xu Y, et al. (2017) VMAT2-Mediated Neurotransmission from Midbrain Leptin Receptor Neurons in Feeding Regulation. eNeuro 4(3):ENEURO.0083-17.2017 |
| abstractText | 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. |
