NKB signaling in the posterodorsal medial amygdala stimulates gonadotropin release in a kisspeptin-independent manner in female mice.

Autor: Fergani C; Department of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Boston, United States.; Harvard Medical School, Boston, United States., Leon S; Department of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Boston, United States.; Harvard Medical School, Boston, United States., Padilla SL; Howard Hughes Medical Institute, University of Washington, Seattle, United States., Verstegen AM; Harvard Medical School, Boston, United States.; Department of Medicine, Division of Endocrinology, Beth Israel Deaconess Medical Center, Boston, United States., Palmiter RD; Howard Hughes Medical Institute, University of Washington, Seattle, United States., Navarro VM; Department of Endocrinology, Diabetes and Hypertension, Brigham and Women's Hospital, Boston, United States.; Harvard Medical School, Boston, United States.
Jazyk: angličtina
Zdroj: ELife [Elife] 2018 Dec 19; Vol. 7. Date of Electronic Publication: 2018 Dec 19.
DOI: 10.7554/eLife.40476
Abstrakt: Neurokinin B (NKB) signaling is critical for reproduction in all studied species. The existing consensus is that NKB induces GnRH release via kisspeptin ( Kiss1 ) stimulation in the arcuate nucleus. However, the stimulatory action of NKB is dependent on circulating estrogen (E 2 ) levels, without which, NKB inhibits luteinizing hormone (LH) release. Importantly, the evidence supporting the kisspeptin-dependent role of NKB, derives from models of persistent hypogonadal state [e.g. Kiss1r knock-out (KO) mice], with reduced E 2 levels. Here, we demonstrate that in the presence of E 2 , NKB signaling induces LH release in a kisspeptin-independent manner through the activation of NK3R (NKB receptor) neurons in the posterodorsal medial amygdala (MePD). Importantly, we show that chemogenetic activation of MePD Kiss1 neurons induces LH release, however, the stimulatory action of NKB in this area is Kiss1 neuron-independent. These results document the existence of two independent neuronal circuitries within the MePD that regulate reproductive function in females.
Editorial Note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (see decision letter).
Competing Interests: CF, SL, SP, AV, VN No competing interests declared, RP Reviewing Editor, eLife
(© 2018, Fergani et al.)
Databáze: MEDLINE
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