课题基金 / 基金详情

Inhibition, Oscillations and Information Processing in Schizophrenia

Inhibition, Oscillations and Information Processing in Schizophrenia
精神分裂症的抑制、振荡和信息处理
批准号:
8105269
负责人:
David A Lewis
金额:
$207.22万
依托单位国家:
美国
项目类别:
财政年份:
2008
资助国家:
美国
项目状态:
已结题
起止时间:
2008-08-01 至 2013-06-30

项目摘要

项目成果

David A Lewis的其他基金

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中文摘要
翻译
精神障碍神经科学中心(CCNMD)提供了一个高度互动的科学环境,整合了来自匹兹堡大学医学院和艺术与科学学院以及邻近的卡内基梅隆大学的多名研究人员的基础和临床研究活动。总的来说,CCNMD代表了跨越分子,系统,认知,计算和临床神经科学的广泛专业知识,为验证GABA神经元亚群中独特的分子改变模式(病理学)引起皮层网络振荡的保守干扰(病理生理学)的中心假设提供了补充方法,这是精神分裂症核心信息处理缺陷(临床综合征)的基础。由行政管理、临床服务和诊断以及统计和数据管理核心支持的5个项目将研究:1)在被认为产生振荡活动的皮层GABA神经元的不同亚群中,精神分裂症患者的分子异常(项目1- lewis);2)综合计算、电生理和解剖学方法,确定细胞类型特异性皮质GABA神经传递与体外振荡的关系(Project 2- ermentrout);3) GABA神经传递在非人类灵长类动物的大脑皮层振荡中所起的作用,这些大脑皮层振荡在精神分裂症中发生了相同的信息加工域的改变(Project 3- olson);4)精神分裂症中特定类型的信息处理障碍与某些皮质区域的激活改变和网络振荡受损有关(Project 4- phillips);5)开发新的PET成像工具,用于体内研究人类皮质GABA神经元的功能(5- mathis项目)。这些项目的协同作用和双向相互作用促进了精神分裂症研究的转化方法,旨在为新的治疗干预确定基于病理生理学的靶点,并开发可用于监测治疗效果的病理生理学生物标志物
英文摘要
This Conte Center for the Neuroscience of Mental Disorders (CCNMD) offers a highly interactive scientific environment that integrates the basic and clinical research activities of multiple investigators from the University of Pittsburgh's Schools of Medicine and Arts and Sciences and the adjacent Carnegie Mellon University. Collectively, the CCNMD represents a broad array of expertise spanning molecular, systems, cognitive, computational and clinical neuroscience that provides complementary approaches to testing the central hypothesis that a distinctive pattern of molecular alterations in subpopulations of GABA neurons (pathology) gives rise to conserved disturbances in cortical network oscillations (pathophysiology) that underlie the core information processing deficits (clinical syndrome) of schizophrenia. The proposed 5 projects, supported by Administrative, Clinical Services and Diagnostics, and Statistics and Data Management Cores, examine 1) molecular abnormalities in schizophrenia in distinct subsets of cortical GABA neurons thought to generate oscillatory activity (Project 1-Lewis); 2) integrated computational, electrophysiological and anatomical approaches to determine the relationship between cell type-specific cortical GABA neurotransmission and oscillations in vitro (Project 2-Ermentrout); 3) the role of GABA neurotransmission in cortical oscillations elicited by tasks that tap in non-human primates the same information processing domains that are altered in schizophrenia (Project 3-Olson); 4) specific types of information processing disturbances in schizophrenia that are linked to altered activation of, and impaired network oscillations in, certain cortical regions (Project 4-Phillips); and 5) the development of new PET imaging tools for studying the function of human cortical GABA neurons in vivo (Project 5-Mathis). The synergism and bi-directional interactions of these projects facilitates a translational approach to schizophrenia research directing at identifying pathophysiology-based targets for novel therapeutic interventions and developing biomarkers of the pathophysiology that can be used to monitor the efficacy of such interventions. Thus, the proposed Center is a multi-disciplinary effort directed at testing a mechanistic hypothesis in order to improve our understanding of a core component of the disease process of schizophrenia. In addition, the Center provides 1) a rich environment for training and career development in which individuals can become involved in studies that bring the methods and knowledge base of basic neuroscience to address critical questions in clinical schizophrenia research, and 2) a mechanism for disseminating the importance of, and the knowledge gained from, translational studies of schizophrenia to the broader scientific and lay communities.
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