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

我的研究项目旨在了解大脑的基本机制，特别是神经元网络，在损伤后重组。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，我使用了一个大鼠全脑缺血模型，模拟在人类心脏骤停或中风后观察到的神经元损伤和功能缺陷。在该大鼠模型中，海马CA1锥体细胞层广泛受损，导致学习记忆缺陷和应激反应。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（即缺血预处理，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方面是，它们在缺血性神经元损伤中没有明显的变化，这表明它们是通过其他神经元回路的改变和/或生化变化诱导的。本研究旨在探讨环境因素引起的功能可塑性和认知改善的一些潜在过程。它的多学科方法将使学生为理解脑损伤后恢复过程的决定因素做出重大贡献。

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.