STRESS ALLOSTASIS: CRF, SEROTONIN AND THE BNST

这个子项目是利用资源的许多研究子项目之一。 由NIH/NCRR资助的中心拨款提供。对子项目的主要支持 子项目的首席调查员可能是由其他来源提供的， 包括美国国立卫生研究院的其他来源。为子项目列出的总成本可能 表示该子项目使用的中心基础设施的估计数量， 不是由NCRR赠款提供给次级项目或次级项目工作人员的直接资金。 2010年，我们总结了我们最初的R01报告中概述的研究(压力同素平衡：CRF、5-羟色胺和BNST)，并成功地应用于NIH继续R01(压力诱导基因调节：BNST、CRF神经元和焦虑的生理学)。我们继续使用反复不可预测的休克应激(USS)方案来检测其对BNST神经元5-羟色胺受体亚型基因表达和离子通道亚单位表达的影响。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》(Hazra等人，2011年出版)上。我们还发表了我们的研究结果，通过生产CRF-GFP转基因小鼠来实现含有CRF的神经元的生理特性(Martin等人，2010年)。另一份手稿正在准备中，描述了BNST中含有CRF的神经元的生理和遗传特性。我们还用这只转基因小鼠检测了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，即CRF神经元支配催产素神经元，反之亦然。这项研究的结果已经提交，目前正在《神经心理内分泌学》杂志上进行审查(Dabrowska等人，提交)。

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).