ORGANOPHOSPHATE NEUROTOXICITY IN EARLY ZEBRAFISH DEVELOPMENT

斑马鱼早期发育中的有机磷酸盐神经毒性

• 批准号: 8167598
• 负责人: KATHLEEN GEORGE
• 金额: $ 1.66万
• 依托单位: UNIVERSITY OF MONTANA
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-06-01 至 2011-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8167598
• 关键词: Acetylcholinesterase; Affect; Axon; Child; Cognition; Cognitive; Computer Retrieval of Information on Scientific Projects Database; Development; Dose; Embryo; Embryonic Development; Exposure to; Funding; Goals; Grant; Institution; Lead; Locomotion; Modeling; Neurologic; O,O-diethyl O-3,5,6-trichloro-2-pyridyl phosphate; Organophosphates; Pathway interactions; Pesticides; Proteins; Research; Research Personnel; Resources; Source; Toxic Environmental Substances; United States National Institutes of Health; Zebrafish; cholinergic; neurotoxicity; pesticide exposure; response; zebrafish development

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Organophosphate pesticides (OPs) are environmental toxins known to inhibit the catalytic activity of acetylcholinesterase (AChE). Developmental exposure to OPs has been hypothesized to disrupt other non-cholinergic pathways in the embryo, such as axon path finding, that lead to locomotion and cognition deficits in young children. In order to understand the neurological pathways affected by OP exposure in the developing vertebrate embryo, we have developed a subacute model of OP developmental exposure in zebrafish. Exposing embryos to a dose of chlorpyrifos oxon (CPO) that is non-lethal allows us to look at potential non-AChE related responses during early embryonic development. Our central hypothesis is that developmental CPO exposure results in changes in axon pathfinding in the developing CNS. The long-term goal of this project is to identify the cellular proteins that CPO modifies that result in the cognitive and locomotion deficits observed in human children who have been exposed to OP.

该副本是利用众多研究子项目之一 由NIH/NCRR资助的中心赠款提供的资源。子弹和 调查员（PI）可能已经从其他NIH来源获得了主要资金， 因此可以在其他清晰的条目中代表。列出的机构是 对于中心，这不一定是调查员的机构。 有机磷酸盐农药（OPS）是已知的环境毒素，可抑制乙酰胆碱酯酶（ACHE）的催化活性。 假设对OPS的发育暴露会破坏胚胎中其他非胆碱能途径，例如轴突路径发现，导致幼儿运动和认知缺陷。为了了解发育中的脊椎动物胚胎中OP暴露影响的神经系统途径，我们开发了斑马鱼中OP发育暴露的亚急性模型。将胚胎暴露于非致命性的一剂毒死rif虫（CPO）中，使我们能够在早期胚胎发育过程中查看潜在的非缓冲反应。 我们的中心假设是，发育CPO暴露会导致发育中心的轴突路径变化。 该项目的长期目标是确定CPO修饰的细胞蛋白，从而导致在暴露于OP的人类儿童中观察到的认知和运动缺陷。