Brain injury and functional plasticity : physiological and environmental factors involved in reorganization of brain functions

脑损伤和功能可塑性：参与脑功能重组的生理和环境因素

• 批准号: 217320-2008
• 负责人: Plamondon, Hélène
• 金额: $ 1.09万
• 依托单位: University of Ottawa
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2010
• 资助国家: 加拿大
• 起止时间: 2010-01-01 至 2011-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=454189
• 关键词: Brain; injury; functional; plasticity; physiological

My research program aims at understanding the basic mechanisms by which the brain in general, and neuronal networks in particular, reorganize following lesion. With my research team, I study the physiological and environmental conditions that promote recovery of function. To study this functional plasticity I use a rat model of global ischemia that mimics the neuronal damage and functional deficits observed in humans following cardiac arrest or stroke. In this rat model, the CA1 pyramidal cell layer of the hippocampus is extensively damaged and this leads to learning and memory deficits and stress reactivity. In the last few years, my students and I have demonstrated that the functional recovery of these deficits can be enhanced by physiological (i.e., ischemic preconditioning, CRH stimulation) and environmental factors such as food restriction and certain nutritional supplements such as fish oil. An interesting aspect of the functional effects seen following exposure to environmental factors is that they take place without apparent changes in ischemic neuronal injury, suggesting that they are induced via alterations of other neuronal circuits and/or biochemical changes. The present research program aims to target some of the processes that may underlay functional plasticity and cognitive improvement induced by environmental factors. Its multidisciplinary approach will prepare students to contribute significantly to understanding the determinants of recovery processes following brain injury.

我的研究项目旨在了解大脑，特别是神经网络在损伤后重组的基本机制。我和我的研究团队一起研究促进功能恢复的生理和环境条件。为了研究这种功能可塑性，我使用了一个全脑缺血的大鼠模型，该模型模拟了人类在心脏骤停或中风后观察到的神经元损伤和功能缺陷。在这种大鼠模型中，海马区CA1锥体细胞层广泛受损，导致学习记忆障碍和应激反应。在过去的几年里，我和我的学生已经证明，这些缺陷的功能恢复可以通过生理因素(即缺血预适应、CRH刺激)和环境因素(如食物限制)和某些营养补充剂(如鱼油)来增强。暴露于环境因素后的功能影响的一个有趣的方面是，它们发生在缺血性神经元损伤没有明显变化的情况下，这表明它们是通过其他神经元电路和/或生化变化的改变而诱导的。目前的研究计划旨在针对一些可能支持环境因素引起的功能可塑性和认知改善的过程。它的多学科方法将使学生准备好为理解脑损伤后恢复过程的决定因素做出重大贡献。