Abstract
The neuropeptides tachykinin2 (Tac2) and kisspeptin (Kiss1) in hypothalamic arcuate nucleus Kiss1 (Kiss1ARH) neurons are essential for pulsatile release of GnRH and reproduction. Since 17b-estradiol (E2) decreases Kiss1 and Tac2 mRNA expression in Kiss1ARHneurons, the role of Kiss1ARHneurons 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 Kiss1ARHneurons 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.
Original language | English (US) |
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Article number | e35656 |
Journal | eLife |
Volume | 7 |
DOIs | |
State | Published - Aug 6 2018 |
ASJC Scopus subject areas
- General Immunology and Microbiology
- General Biochemistry, Genetics and Molecular Biology
- General Neuroscience