| First Author | Qiu J | Year | 2018 |
| Journal | Elife | Volume | 7 |
| PubMed ID | 30079889 | Mgi Jnum | J:269821 |
| Mgi Id | MGI:6269109 | Doi | 10.7554/eLife.35656 |
| Citation | Qiu J, et al. (2018) Estrogenic-dependent glutamatergic neurotransmission from kisspeptin neurons governs feeding circuits in females. Elife 7:e35656 |
| abstractText | The neuropeptides tachykinin2 (Tac2) and kisspeptin (Kiss1) in hypothalamic arcuate nucleus Kiss1 (Kiss1(ARH)) neurons are essential for pulsatile release of GnRH and reproduction. Since 17beta-estradiol (E2) decreases Kiss1 and Tac2 mRNA expression in Kiss1(ARH) neurons, the role of Kiss1(ARH) neurons during E2-driven anorexigenic states and their coordination of POMC and NPY/AgRP feeding circuits have been largely ignored. Presently, we show that E2 augmented the excitability of Kiss1(ARH) neurons by amplifying Cacna1g, Hcn1 and Hcn2 mRNA expression and T-type calcium and h-currents. E2 increased Slc17a6 mRNA expression and glutamatergic synaptic input to arcuate neurons, which excited POMC and inhibited NPY/AgRP neurons via metabotropic receptors. Deleting Slc17a6 in Kiss1 neurons eliminated glutamate release and led to conditioned place preference for sucrose in E2-treated KO female mice. Therefore, the E2-driven increase in Kiss1 neuronal excitability and glutamate neurotransmission may play a key role in governing the motivational drive for palatable food in females. |
