GENES CONTROLLING PUBERTY ONSET

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 目的：研究控制青春期发育的基因。 了解青春期在大脑中的机制很重要，因为一些疾病和行为障碍与青春期有关。 在这项研究中，我们研究了Kispeptin在青春期LHRH释放增加中的作用。结果表明，用微透析法测量的Kispeptin-54在柄-正中隆起中的释放是搏动性的，在青春期开始时，平均Kispeptin-54的水平和脉冲频率增加，但脉冲幅度不变。此外，青春期Kispeptin-54的释放增加与青春期循环卵巢雌激素的变化无关，因为青春期去卵巢的女性也观察到了Kispeptin-54的释放增加。最后，通过评估LHRH对KP激动剂和拮抗剂KP-10和肽234的反应，研究了GPR54对KP敏感性的发育变化。初步结果表明，LHRH对KP-10或234肽的反应在青春期前和青春期组之间都不同，表明GPr54敏感性没有发生发育变化。总体而言，这些结果与Kispeptin在青春期起作用的假设是一致的。 这项研究使用了WNPRC动物服务和化验服务。 出版物： Roseweir，A.K.，Kauffman，A.S.，Smith，J.T.，Guerriero，K.A.，Morgan，K.，Pielecka-ForTuna，J.，Pineda，R.，Gottsch，M.L.，Tena-Sempere，M.，Moenter，S.M.，Terasawa，E.，Clarke，I.J.，Steiner，R.A.和Millar，R.P.J.神经学29：3920-3929,2009。PMID：19321788

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Objective: To investigate genes controlling the timing of puberty. Understanding the mechanism of puberty in the brain is important, as some diseases and behavioral disturbances occur in association with puberty. In this study the role of kisspeptin in the pubertal increase in LHRH release was examined. The results suggest that kisspeptin-54 release in the stalk-median eminence measured by a microdialysis method was pulsatile and mean kisspeptin-54 levels and pulse frequency, but not pulse amplitude, increased at the onset of puberty. Moreover, the pubertal increase in kisspeptin-54 release was independent from the pubertal changes in circulating ovarian estrogen, as the pubertal increase in kisspeptin-54 release was also observed in ovariectomized females. Finally, developmental changes in GPR54 sensitivity to KP were examined by assessing the LHRH response to a KP agonist and antagonist, KP-10 and peptide 234, respectively. Preliminary results suggest that the LHRH response to neither KP-10 nor peptide 234 was different between prepubertal and pubertal groups, indicating that GPR54 sensitivity does not undergo developmental changes. Collectively, the results are consistent with the hypothesis that kisspeptin plays a role in puberty. This research used WNPRC Animal Services and Assay Services. PUBLICATION: Roseweir, A.K., Kauffman, A.S., Smith, J.T., Guerriero, K.A., Morgan, K., Pielecka-Fortuna, J., Pineda, R., Gottsch, M.L., Tena-Sempere, M., Moenter, S.M., Terasawa, E., Clarke, I.J., Steiner, R.A., and Millar, R.P. Discovery of potent kisspeptin antagonists delineate physiological mechanisms of gonadotropin regulation. J. Neurosci. 29:3920-3929, 2009. PMID: 19321788