Acute and Chronic Stress, Neurobehavior and Drug Abuse

急性和慢性压力、神经行为和药物滥用

• 批准号: 6919005
• 负责人: TIMOTHY C BLACKSON
• 金额: $ 3.99万
• 依托单位: UNIVERSITY OF PITTSBURGH AT PITTSBURGH
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-04-01 至 2005-10-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6919005
• 关键词: adolescence (12-20); behavioral /social science research tag; behavioral genetics; biomarker; clinical research; disease /disorder proneness /risk; family structure /dynamics; human subject; hypothalamic pituitary adrenal axis; impulsive behavior; longitudinal human study; middle childhood (6-11); neuropsychological tests; neuropsychology; startle reaction; stress; substance abuse epidemiology; substance abuse related disorder; young adult human (21-34)

DESCRIPTION (provided by applicant): The goals for this 3-year Mentored Research Scientist Development Award (K01) application are to: (1) Re-establish an investigative career after the hiatus necessitated by attending to my wife's fatal illness; (2) Upgrade my research skills pertaining to methodology for researching the effects of acute stress on the liability to DSM-IV substance use disorders (SUD); and, (3) Devote full time effort to research without clinical or teaching duties, and limiting organizational duties to research conducted at the NIDA-funded Center for Education and Drug Abuse (CEDAR) which has been funded through April 2009. My research project will elucidate the role of acute stress reactivity in a cohort of young adults (N=160) age 22, in a modal period of maximum lifetime risk for developing SUD. Participants are recruited from an ongoing prospective investigation of SUD under the aegis of the NIDA-funded CEDAR and have already been studied in four prior waves of biobehavioral data collection conducted at ages 10-12, 12-14, 16 and 19. This project will delineate the conjoint impact of three putative SUD risk factors: (1) parental phenotype (parental SUD+/parental SUD-), (2) offspring's neurobehavior disinhibition (ND); and, 3) acute stress reactivity in controlled laboratory studies using physiological and psychological measurements. Through the education and training component I will acquire the expertise to document stress reactivity via hypothalamic-pituitary-adrenal axis (HPA) activity and acoustical startle reflex (electromyograms). Specifically, I will acquire the research skills to: (1) Determine the extent to which exposure to acute stress impacts on the relationship between neurobehavior disinhibition (a SUD liability phenotype) and severity of substance use and (2) Clarify the extent to which stress reactivity impacts on the relationship between parental SUD and their offspring's ND. Elucidating the role of stress by taking into account its acute facets along with individual variation in neurobehavioral vulnerability, will point to innovative strategies for prevention and treatment of SUD. By mid-Year 03, I will prepare an R01 application directed at conducting a longitudinal stress study to inform on prevention strategies.

描述（由申请人提供）： 这项为期 3 年的指导研究科学家发展奖（K01）申请的目标是：（1）在因照顾我妻子的致命疾病而中断后重新建立调查职业； (2) 提升我的研究技能，涉及研究急性压力对 DSM-IV 物质使用障碍 (SUD) 的影响的方法； (3) 全身心投入研究，但不承担临床或教学职责，并将组织职责限制在 NIDA 资助的教育和药物滥用中心 (CEDAR) 进行的研究，该中心的资助截至 2009 年 4 月。 我的研究项目将阐明急性应激反应在一群 22 岁的年轻人 (N=160) 中的作用，这些年轻人处于患 SUD 的最大终生风险的最典型时期。参与者是从 NIDA 资助的 CEDAR 主持下正在进行的 SUD 前瞻性调查中招募的，并且已经在 10-12、12-14、16 和 19 岁进行的四轮生物行为数据收集中进行了研究。该项目将描述三个假定的 SUD 风险因素的联合影响：(1) 亲代表型（亲代 SUD+/亲代 SUD-），(2)后代的神经行为去抑制（ND）； 3）使用生理和心理测量的受控实验室研究中的急性应激反应。 通过教育和培训部分，我将获得通过下丘脑-垂体-肾上腺轴 (HPA) 活动和声惊吓反射（肌电图）记录压力反应性的专业知识。具体来说，我将获得以下研究技能：(1) 确定暴露于急性压力对神经行为去抑制（SUD 责任表型）和物质使用严重程度之间关系的影响程度，以及 (2) 澄清压力的程度反应性影响亲本 SUD 与其后代 ND 之间的关系。通过考虑压力的急性方面以及神经行为脆弱性的个体差异来阐明压力的作用，将为预防和治疗 SUD 提供创新策略。到第三年年中，我将准备一份 R01 申请，旨在进行纵向压力研究，以告知预防策略。