MOLECULAR AND STRUCTURAL BASES OF HYPOTHALAMIC PUBERTY

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。 这是一个旨在了解导致人类青春期开始的生理机制的项目。在Ojeda博士的实验室中进行的研究是在主要应用的特定目标3下提出的。目的：在没有干扰睾丸激素反馈的情况下，确定下丘脑基因表达的整体情况：1)婴儿期GnRH脉动性释放受到抑制，2)幼年发育末期GnRH脉动性释放回升。恒河猴将被用作实验范例。标准的生理学模型将被用来检验GPR54信号的增加是否会维持GnRH的早熟释放。下丘脑内注射神经内切酶可以防止结构重构，候选基因和全局基因的表达将分别通过RNase保护和包含8,400个人cDNA(或8,000-10,000个猴子cDNA)的基因阵列进行检测。

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. This is a project aimed to understanding the physiological mechanisms responsible for the onset of puberty in humans. Studies performed in Dr. Ojeda's lab are those proposed under Specific Aim 3 of the main application. Aim 3: To determine, in the absence of interfering testicular hormone feedback, the global profile of hypothalamic gene expression at the time of 1) the suppression of pulsatile GnRH release during infancy, and 2) the resurgence in pulsatile GnRH release at the end of the juvenile phase of development. The rhesus monkey will be used as an experimental paradigm. Standard physiological models will be used to examine whether increased GPR54 signaling will sustain precocious GnRH release. Structural remodeling will be prevented by intrahypothalamic injection of endoneurominidase, and candidate and global gene expression will be examined by RNAse protection and hybridization to gene arrays containing 8,400 human cDNAs (or 8,000-10,000 monkey cDNAs), respectively.