DIST & QUANTIF OF SEROTONIN 1A RECEPTORS IN DEPRESSED SUBJECTS W/PET

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。 重度抑郁症是一种常见的致残性疾病，被认为是由脑细胞之间的化学通讯(神经传递)的变化所介导的。众所周知，压力和消极的生活事件会引发严重抑郁症的发作，然后往往需要一个重复的、自主的过程。随着随后的抑郁发作再次发生，其治疗往往变得更加困难，压力和抑郁发作之间的联系变得不那么明显。 这个项目研究了神经递质系统的功能，即5-羟色胺能，它与情绪调节和抗抑郁药物的效果有关。它研究了对压力反应的激素(糖皮质激素和盐皮质激素)和5-羟色胺1A受体浓度之间的关系，5-羟色胺1A受体介导了5-羟色胺在脑细胞中的一些作用。据推测，这些应激反应激素的异常(增加)产生将影响5-羟色胺1A受体的浓度，而这将反过来与抗抑郁药物的不良反应有关。阐明这些机制将提高我们对严重抑郁的大脑基础以及个体对抗抑郁药物反应的差异性的理解。

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. Major Depression is a frequent and disabling illness, thought to be mediated by changes in the chemical communication (neurotransmission) between brain cells. Stress and negative life events are known to precipitate the onset of episodes of Major Depression, which then often takes a repetitive, autonomous course. As subsequent episodes of depression re-occur, its treatment often times becomes more difficult, and the association between stress and episodes of depression becomes less apparent. This project examines the function of a neurotransmitter system, the serotonergic, implicated in the regulation of mood and in the effect of antidepressant medications. It examines the relationship between hormones responsive to stress (glucocorticoids and mineralocorticoids), and the concentration of serotonin 1A receptors, which mediate some of the effects of serotonin in brain cells. It is hypothesized that the abnormal (increased) production of these stress-response hormones will influence the concentration of serotonin 1A receptors, which will in turn be associated with a poor response to antidepressant medications. Elucidation of these mechanisms will improve our understanding of the brain underpinnings of Major Depression and the variability in the individual's response to antidepressants.'