MECHANISMS OF HYPEROXIA-INDUCED DEVELOPMENTAL PLASTICITY OF RESPIRATORY CONTROL

高氧诱导呼吸控制发育可塑性的机制

• 批准号: 7381452
• 负责人: RYAN W BAVIS
• 金额: $ 14.61万
• 依托单位: MOUNT DESERT ISLAND BIOLOGICAL LAB
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-05-01 至 2007-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7381452
• 关键词: MECHANISMS; HYPEROXIA; INDUCED; DEVELOPMENTAL; PLASTICITY

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. The perinatal environment influences development of the respiratory control system in mammals and birds. We have been studying a model of developmental plasticity in which rats are exposed to hyperoxia (60% oxygen) during the first 1-4 postnatal weeks. These rats exhibit permanently attenuated ventilatory responses to acute hypoxia owing to abnormal development of the carotid body. Our project is investigating the cellular and molecular mechanisms by which elevated oxygen influences carotid body development. Experiments conducted in this reporting period aim to determine whether hyperoxia attenuates ventilatory reflexes in birds as previously observed in mammals. These experiments will enable us to evaluate precocial birds as a model for embryonic hyperoxia that is free from maternal effects inherent to studies of placental mammals. Initial studies refined methodology for hyperoxia exposures and ventilation measurements in birds, and now ventilatory reflexes are being studied in adult quail following embryonic and postnatal exposure to chronic hyperoxia. Additional ongoing experiments are evaluating the role of reactive oxygen species in hyperoxia-induced developmental plasticity. Specifically, these experiments are designed to assess (1) whether our model of hyperoxia elicits cellular damage attributable to reactive oxygen species and (2) whether antioxidants can prevent changes in carotid body functional development during perinatal hyperoxia. Other accomplishments during this reporting period include hiring a full-time Research Assistant and developing the capacity to conduct acute neurophysiological experiments in our laboratory.

该子项目是利用NIH/NCRR资助的中心赠款提供的资源的许多研究子项目之一。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。列出的机构适用于该中心，这不一定是调查员的机构。围产期环境影响哺乳动物和鸟类呼吸控制系统的发展。我们一直在研究一种发育可塑性模型，在该模型中，大鼠在最初的1-4个星期后暴露于高氧（60％氧）。由于颈动脉体的异常发育，这些大鼠表现出对急性缺氧的通气反应永久减弱。我们的项目正在研究氧气影响颈动脉体发育的细胞和分子机制。在本报告期间进行的实验旨在确定高氧是否如前在哺乳动物中观察到的鸟类中的通气反射能力减弱。这些实验将使我们能够评估早熟鸟作为胚胎高氧的模型，而胚胎哺乳动物研究固有的母体影响。初步研究完善了鸟类中高氧暴露和通风测量的方法，现在在胚胎和产后暴露于慢性高氧后的成年鹌鹑中正在研究通气反射。其他正在进行的实验是评估活性氧在高氧引起的发育可塑性中的作用。具体而言，这些实验旨在评估（1）我们的高氧模型是否会引起可归因于活性氧的细胞损伤以及（2）抗氧化剂是否可以防止围产期高氧期间颈动脉体功能发育的变化。在此报告期间，其他成就包括聘请一名全日制研究助理，并在我们的实验室中开发进行急性神经生理实验的能力。