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).

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