Core-A Administative

这个康特精神疾病神经科学中心(CCNMD)提供了一个高度互动的科学 整合了多名来自 匹兹堡大学医学院、文理学院和邻近的卡内基梅隆大学 大学。总的来说，CCNMD代表了一系列广泛的专业知识，涵盖分子、系统、 认知、计算和临床神经科学，提供测试的补充方法 中心假设：GABA神经元亚群中一种独特的分子变化模式 (病理学)在皮质网络振荡(病理生理学)中引起保守的干扰 精神分裂症的核心信息处理缺陷(临床综合征)。建议的5 由行政、临床服务和诊断以及统计和数据支持的项目 管理核心，检查1)精神分裂症患者大脑皮质不同亚群的分子异常 被认为产生振荡活动的GABA神经元(项目1-Lewis)；2)集成计算， 电生理和解剖学方法确定细胞类型特异性之间的关系 皮质GABA神经传递和体外振荡(项目2-Ermentrout)；3)GABA的作用 在非人类灵长类动物中利用同样的任务诱发的皮质振荡的神经传递 精神分裂症患者改变的信息处理领域(项目3-Olson)；4)特定类型的 精神分裂症患者的信息处理障碍与激活和受损的改变有关 某些皮质区域的网络振荡(项目4-菲利普斯)；以及5)新PET的发展 研究活体人类皮质GABA神经元功能的成像工具(项目5-Mathis)。这个 这些项目的协同和双向互动促进了一种翻译方法 精神分裂症研究旨在确定基于病理生理学的新治疗靶点 干预和开发可用于监测疗效的病理生理学生物标记物 这样的干预。因此，拟议的中心是一个多学科的努力，旨在测试一个机械 假说，以提高我们对疾病过程的一个核心组成部分的理解 精神分裂症。此外，该中心还提供1)丰富的培训和职业发展环境 哪些人可以参与到研究中来，带来基本的方法和知识基础 神经科学来解决临床精神分裂症研究中的关键问题，以及2)一种机制 将精神分裂症翻译研究的重要性和知识传播到 更广泛的科学界和非科学界。

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.