HPA Axis in Depression and Anxiety

HPA 轴在抑郁和焦虑中的作用

• 批准号: 6330748
• 负责人: ELIZABETH ANN YOUNG
• 金额: $ 12.83万
• 依托单位: UNIVERSITY OF MICHIGAN AT ANN ARBOR
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-05-01 至 2006-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6330748
• 关键词: anxiety disorders; clinical depression; clonidine; comorbidity; cortisol; hormone regulation /control mechanism; human subject; hypothalamic pituitary adrenal axis; norepinephrine; panic disorder; patient oriented research; physiologic stressor; posttraumatic stress disorder; psychological stressor; psychological tests; somatotropin; urinalysis

DESCRIPTION: (Applicant's abstract) This is a Research Scientist Award Application. I have received 15 years of salary support through the RSDA program and have become a leader in the area of HPA axis regulation in depression. Future studies proposed in this application will continue to explore hormonal abnormalities in depression and also in related anxiety disorders, panic disorder and PTSD. Current research indicates that depression is accompanied by abnormalities of the HPA axis, while anxiety disorders, particularly Panic Disorder, is accompanied by abnormalities of the central noradrenergic system, as reflected by a blunted growth hormone response to clonidine. Specific research aims in this proposal are I) to determine if abnormalities of central noradrenergic system are present in both pure depression, pure panic disorder and depression plus panic disorder. We will study a group of well characterized pure depressed, pure panic and mixed panic and depressed patients with the clonidine/growth hormone challenge to determine if all depressed patients manifest abnormalities in clonidine stimulated growth hormone release or if only those with co-morbid panic symptoms manifest this abnormality. 2) To determine if abnormal activation of HPA axis secretion occurs in Panic Disorder patients. We will examine 24 hr urinary cortisol excretion, collected in 8 hrs segments in pure depressed, pure panic and and mixed panic and depressed patients. 3) To evaluate noradrenergic and HPA axis 'reactivity' to two simple challenges in pure depression, depression plus anxiety, panic disorder patients and normal controls. These challenges include orthostatic challenge and the Trier Social Stress Test (TSST). We hypothesize that panic disorder patients and depressed patients with co-morbid anxiety will demonstrate exaggerated catecholamine response to orthostatic challenge i.e increased reactivity. We hypothesize that depressed patients will have altered HPA axis responses to stress response while Panic Disorder patients will have normal HPA axis response to the TSST. 4 ) To determine if the abnormalities in basal HPA axis dysregulation, exaggerated responses to stress and blunted response to clonidine-growth hormone challenge studies occur in the same individuals and if the results of these biological studies support the nosological distinction between Panic Disorder, pure Major Depression and Major Depression with co-morbid Panic Disorder. Finally we will examine whether HPA axis and noradrenergic dysfunction reflect a common factor, degree of impairment, more than a specific mood and anxiety disorder. With regards to PTSD, we will explore whether decreases in urinary free cortisol and increases in urinary catecholamines are present in epidemiological sample of subjects exposed to trauma both with and without PTSD and normal subjects not exposed to trauma who are free of Psychiatric disorders.

描述：（申请人摘要）这是一个研究科学家奖