OXYTOCIN, VASOPRESSIN & SOCIAL BEHAVIOR IN NON HUMAN PRIMATES

催产素、加压素

• 批准号: 6288142
• 负责人: JAMES Timothy WINSLOW
• 金额: $ 8.4万
• 依托单位: EMORY UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 1999
• 资助国家: 美国
• 起止时间: 1999-05-01 至 2000-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6288142
• 关键词: Mammalia; behavioral /social science research tag; cognition; nervous system; psychology

Several recent studies have demonstrated that central oxytocin and vasopressin pathways are important for species typical social behaviors in rodents. This proposal extends this work to non-human primates by investigating oxytocin and vasopressin in both normal and socially abnormal rhesus monkeys. Proposed studies will characterize the social and cognitive deficits in these monkeys, investigate the influence of centrally administered agonists and antagonists, and in post-mortem studies, assess oxytocin and vasopressin function with cellular and molecular techniques. As many of the behavioral deficits in these socially abnormal monkeys resemble the core features of autism and the deficit syndrome of schizophrenia, the results from the proposed studies may provide pathophysiologic insights and novel medications for these treatment-refractory syndromes. We have recently completed a series of studies of face recognition by rhesus monkeys using the computer assisted paradigm developed with Lisa Parr and Bill Hopkins. We have recently received notice of the successful application for funding for further studies of this topic from NIMH. Animals for these studies will be recruited this year. FUNDING Yerkes / Venture $20,000 1/01/98 - 12/31/99 PUBLICATIONS None

最近的几项研究表明，中枢催产素和 加压素途径对于物种典型的社会性很重要 啮齿动物的行为。 该提案将这项工作扩展到非人类 通过研究正常和灵长类动物中的催产素和加压素 社会异常的恒河猴。 拟议的研究将描述 这些猴子的社交和认知缺陷，调查 中枢给药的激动剂和拮抗剂的影响，以及 尸检研究，评估催产素和加压素功能 细胞和分子技术。 由于许多行为缺陷 这些社会异常的猴子的核心特征类似于 自闭症和精神分裂症的缺陷综合症，结果 拟议的研究可能提供病理生理学见解和新颖的 用于治疗这些难治性综合征的药物。 我们有 最近完成了恒河猴人脸识别的一系列研究 猴子使用与 Lisa Parr 一起开发的计算机辅助范例 和比尔·霍普金斯。 最近我们收到了成功的通知 向 NIMH 申请进一步研究该主题的资金。 这些研究的动物将于今年招募。 资助耶克斯 / Venture $20,000 1/01/98 - 12/31/99 出版物 无