STRESS ALLOSTASIS: CRF, SEROTONIN AND THE BNST

应激失衡：CRF、血清素和 BNST

• 批准号: 8357415
• 负责人: DONALD G RAINNIE
• 金额: $ 3.29万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-08-01 至 2012-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8357415
• 关键词: Anxiety; Cells; Foundations; Funding; Gene Expression; Gene Expression Regulation; Genetic; Grant; Hypothalamic structure; Ion Channel; Manuscripts; Molecular; National Center for Research Resources; Neurons; Neuropeptides; Neurosciences; Oxytocin; Physiological; Physiology; Preparation; Primates; Principal Investigator; Production; Property; Protocols documentation; Publishing; Research; Research Design; Research Infrastructure; Resources; Serotonin; Shock; Source; Stress; System; Transgenic Mice; United States National Institutes of Health; Work; allostasis; cost; serotonin receptor

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. Primary support for the subproject and the subproject's principal investigator may have been provided by other sources, including other NIH sources. The Total Cost listed for the subproject likely represents the estimated amount of Center infrastructure utilized by the subproject, not direct funding provided by the NCRR grant to the subproject or subproject staff. In 2010 we concluded the studies outlined in our original R01 submission (Stress Allostasis: CRF, Serotonin and the BNST) and successfully applied to NIH for continuation R01 (Stress-Induced Gene Regulation: BNST CRF Neurons and the Physiology of Anxiety). We have continued to work with the repeated unpredictable shock stress (USS) protocol to examine its effects on the gene expression of serotonin receptor subtypes as well as ion channel subunit expression in BNST neurons. As a foundation for these studies we have conducted a study designed to look at the cell-specific expression of four key ion channel subunits, namely those of Ih, IT, IA, and IAR. The results of these studies were recently published in Molecular and Cellular Neuroscience (Hazra et al., 2011, In Press). We have also published the results of our studies into the physiological properties of CRF-containing neurons that were made possible through the production of a CRF-GFP transgenic mouse (Martin et al., 2010). Another manuscript is in preparation describing the physiological and genetic properties of CRF-containing neurons in the BNST. We have also used this transgenic mouse to examine the relationship between BNST CRF neurons and oxytocin-containing neurons in the hypothalamus. Our studies have revealed a reciprocal relationship between these two neuropeptide systems, such that CRF neurons innervate the oxytocin neurons, and vice versa. The results of this study were submitted and are current under review in Neuropsychoendocrinology (Dabrowska et al., submitted).

该子项目是利用资源的众多研究子项目之一 由 NIH/NCRR 资助的中心拨款提供。子项目的主要支持 并且子项目的首席研究员可能是由其他来源提供的， 包括其他 NIH 来源。 子项目可能列出的总成本 代表子项目使用的中心基础设施的估计数量， NCRR 赠款不直接向子项目或子项目工作人员提供资金。 2010 年，我们完成了最初提交的 R01（压力失衡：CRF、血清素和 BNST）中概述的研究，并成功向 NIH 申请了延续 R01（压力诱导基因调节：BNST CRF 神经元和焦虑生理学）。 我们继续使用重复的不可预测的冲击应激（USS）方案来检查其对 BNST 神经元中血清素受体亚型的基因表达以及离子通道亚基表达的影响。 作为这些研究的基础，我们进行了一项研究，旨在观察四个关键离子通道亚基（即 Ih、IT、IA 和 IAR）的细胞特异性表达。这些研究的结果最近发表在《分子和细胞神经科学》上（Hazra 等人，2011 年，出版中）。 我们还发表了对含有 CRF 的神经元的生理特性的研究结果，这些神经元是通过生产 CRF-GFP 转基因小鼠而成为可能的（Martin 等人，2010）。另一份手稿正在准备中，描述 BNST 中含有 CRF 的神经元的生理和遗传特性。 我们还使用这种转基因小鼠来检查 BNST CRF 神经元和下丘脑中含有催产素的神经元之间的关系。 我们的研究揭示了这两个神经肽系统之间的相互关系，例如 CRF 神经元支配催产素神经元，反之亦然。这项研究的结果已提交，目前正在神经精神内分泌学杂志上进行审查（Dabrowska 等人，已提交）。