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Because both studies involved congenital absence of Kiss1r, it becomes important to block endogenous kisspeptin signaling in nongenetically modified animals and determine whether positive-feedback responses persist. E2 treatment induced LH surges in Kiss1r −/− mice in one study ( 12) but did not in another ( 11). Further studies in sheep ( 6, 7) and primates ( 8) show kisspeptin cells in the POA may also play a role in generating the estrogen positive-feedback preovulatory GnRH/LH surge.ĭisabling mutations or genetic deletions of the kisspeptin receptor gene ( Kiss1r) result in the failure to reach puberty ( 9, 10), but there is disagreement as to whether mice with null mutations in Kiss1r are able to mount an estrogen positive-feedback response and LH surge ( 11, 12). Kisspeptin cells in the ovine ARC appear to be involved in positive-feedback regulation of GnRH ( 4) and also appear to be important for negative-feedback regulation of GnRH secretion ( 5). In sheep, kisspeptin cells are located in the dorsolateral preoptic area (POA) and arcuate nucleus (ARC) ( 3). Thus, kisspeptin appears important for both the negative- and positive-feedback signals of estradiol (E2). Kisspeptin cells in the brain have proven to be a conduit for gonadal steroid feedback control of GnRH secretion ( 1, 2).
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Kisspeptin neurons of the ARC project to the external zone of the ME and kisspeptin acts upon the GnRH fibers at this level.
WHAT OTHER PROGRAM IS EQUAL TO NEUROTRACKER SYSTEM THE AUC FULL
Overall, these data indicate an essential role for kisspeptin in receiving stimulatory estrogen signals and generating the full positive feedback GnRH/LH surge. This suggests direct kisspeptin to GnRH terminal-to-terminal communication within the ME. Finally, we showed kisspeptin stimulates GnRH release from ovine ME-cultured explants. ARC populations of kisspeptin neurons project fibers to the ME. To examine alternative pathways for kisspeptin stimulation of GnRH neurons, we examined the origin of kisspeptin neuronal fibers in the external zone of the median eminence (ME) using neuronal tracing and immunohistochemical techniques. Kiss1r mRNA expression in GnRH neurons was also similar across the estrous cycle. Kisspeptin significantly stimulated GnRH secretion into the hypophysial portal system, but the response to kisspeptin was similar in luteal and late-follicular phase ewes. We further examined the response to kisspeptin treatment prior to the LH surge. Kisspeptin antagonist treatment significantly attenuated these LH surges.
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To determine the role of kisspeptin in transmitting estrogen-positive feedback in the hypothalamus, we administered the kisspeptin antagonist p-271 to ewes subjected to an estradiol benzoate-induced LH surge. In sheep, Kiss1 mRNA-expressing cells are found in the arcuate nucleus (ARC) and dorsal-lateral preoptic area and both appear to mediate the positive feedback effect of estradiol to generate the preovulatory GnRH/LH surge. Kisspeptins are the product of the Kiss1 gene and potently stimulate GnRH secretion.