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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 17β-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.

Estrogenic-dependent glutamatergic neurotransmission from kisspeptin neurons governs feeding circuits in females