Send to

Choose Destination
Elife. 2018 Aug 6;7. pii: e35656. doi: 10.7554/eLife.35656.

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

Author information

Department of Physiology and Pharmacology, Oregon Health and Science University, Portland, United States.
Department of Biochemistry, Howard Hughes Medical Institute, University of Washington, Seattle, United States.
Division of Neuroscience, Oregon National Primate Research Center, Oregon Health and Science University, Beaverton, United States.


The neuropeptides tachykinin2 (Tac2) and kisspeptin (Kiss1) in hypothalamic arcuate nucleus Kiss1 (Kiss1ARH) neurons are essential for pulsatile release of GnRH and reproduction. Since 17β-estradiol (E2) decreases Kiss1 and Tac2 mRNA expression in Kiss1ARH neurons, the role of Kiss1ARH 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 Kiss1ARH 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.


17-beta-estradiol; T-type calcium current; h-current; mouse; neuroscience; optogenetics; vGluT2

[Indexed for MEDLINE]
Free PMC Article

Conflict of interest statement

JQ, HR, MB, SP, TS, MK, OR No competing interests declared, RP Reviewing editor, eLife

Supplemental Content

Full text links

Icon for eLife Sciences Publications, Ltd Icon for PubMed Central
Loading ...
Support Center