Kisspeptin and Neurokinin B Signaling Network Underlies the Pubertal Increase in GnRH Release in Female Rhesus Monkeys.

Autor:	Garcia JP; Wisconsin National Primate Research Center, Madison, Wisconsin 53715., Guerriero KA; Wisconsin National Primate Research Center, Madison, Wisconsin 53715., Keen KL; Wisconsin National Primate Research Center, Madison, Wisconsin 53715., Kenealy BP; Wisconsin National Primate Research Center, Madison, Wisconsin 53715., Seminara SB; Reproductive Endocrine Unit and the Harvard Reproductive Sciences Center, Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts 02114., Terasawa E; Wisconsin National Primate Research Center, Madison, Wisconsin 53715.; Department of Pediatrics, University of Wisconsin-Madison, Madison, Wisconsin 53706.
Jazyk:	angličtina
Zdroj:	Endocrinology [Endocrinology] 2017 Oct 01; Vol. 158 (10), pp. 3269-3280.
DOI:	10.1210/en.2017-00500
Abstrakt:	Loss-of-function or inactivating mutations in the genes coding for kisspeptin and its receptor (KISS1R) or neurokinin B (NKB) and the NKB receptor (NK3R) in humans result in a delay in or the absence of puberty. However, precise mechanisms of kisspeptin and NKB signaling in the regulation of the pubertal increase in gonadotropin-releasing hormone (GnRH) release in primates are unknown. In this study, we conducted a series of experiments infusing agonists and antagonists of kisspeptin and NKB into the stalk-median eminence, where GnRH, kisspeptin, and NKB neuroterminal fibers are concentrated, and measuring GnRH release in prepubertal and pubertal female rhesus monkeys. Results indicate that (1) similar to those previously reported for GnRH stimulation by the KISS1R agonist (i.e., human kisspeptin-10), the NK3R agonist senktide stimulated GnRH release in a dose-responsive manner in both prepubertal and pubertal monkeys; (2) the senktide-induced GnRH release was blocked in the presence of the KISS1R antagonist peptide 234 in pubertal but not prepubertal monkeys; and (3) the kisspeptin-induced GnRH release was blocked in the presence of the NK3R antagonist SB222200 in the pubertal but not prepubertal monkeys. These results are interpreted to mean that although, in prepubertal female monkeys, kisspeptin and NKB signaling to GnRH release is independent, in pubertal female monkeys, a reciprocal signaling mechanism between kisspeptin and NKB neurons is established. We speculate that this cooperative mechanism by the kisspeptin and NKB network underlies the pubertal increase in GnRH release in female monkeys. (Copyright © 2017 Endocrine Society.)
Databáze:	MEDLINE
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