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，特别是神经网络在损伤后重组的基本机制。与我的研究团队一起，我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，我使用了大鼠模型的全脑缺血，模仿神经元损伤和功能缺陷，在人类心脏骤停或中风后观察。 在该大鼠模型中，海马的CA 1锥体细胞层广泛受损，这导致学习和记忆缺陷以及应激反应。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。暴露于环境因素后观察到的功能效应的一个有趣的方面是，它们在缺血性神经元损伤中没有明显变化，这表明它们是通过改变其他神经元回路和/或生化变化诱导的。本研究计划的目的是针对一些过程，可能会阻碍功能可塑性和认知改善的环境因素引起的。 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.