GENES CONTROLLING PUBERTY ONSET

该子项目是利用 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 中心，不一定是研究者的机构。 目的：探讨控制青春发育时间的基因。 了解大脑中青春期的机制是很重要的，因为一些疾病和行为障碍与青春期有关。 在这项研究中，Kisspeptin在青春期LHRH释放增加的作用进行了研究。结果表明，kisspeptin-54释放的茎正中隆起测量的微透析方法是脉动的，平均kisspeptin-54水平和脉冲频率，但不是脉冲幅度，在青春期开始增加。此外，青春期kisspeptin-54释放的增加与青春期卵巢雌激素循环的变化无关，因为在卵巢切除的女性中也观察到青春期kisspeptin-54释放的增加。最后，通过评估LHRH对KP激动剂和拮抗剂KP-10和肽234的反应，分别检查GPR 54对KP敏感性的发育变化。 初步结果表明，LHRH的反应既不KP-10也不肽234是青春期前和青春期组之间的不同，表明GPR 54的敏感性不经历发育的变化。总的来说，研究结果与kisspeptin在青春期发挥作用的假设一致。 本研究使用WNPRC Animal Services和Assay Services。 出版物： Roseweir，A.K.，考夫曼，A. S.，史密斯，J.T.，Guerriero，K.A.，摩根，K.，Pielecka-Pieleca，J.，皮内达河Gottsch，M.L.，Tena-Sempere，M.，Moenter，S.M.，Terasawa，E.，克拉克，I. J.，Steiner，R.A.，和Millar，R.P. Discovery of potent kisspeptin antagonists delineate physiological mechanisms of gonadotropin regulation.神经科学杂志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