Interactions of neural plasticity and behavior

神经可塑性和行为的相互作用

• 批准号: 205031-2006
• 负责人: Corcoran, Michael
• 金额: $ 2.55万
• 依托单位: University of Saskatchewan
• 依托单位国家: 加拿大
• 项目类别: Discovery Grants Program - Individual
• 财政年份: 2007
• 资助国家: 加拿大
• 起止时间: 2007-01-01 至 2008-12-31
• 项目状态: 已结题
• 来源: https://www.nserc-crsng.gc.ca/ase-oro/Details-Detailles_eng.asp?id=361518
• 关键词: Interactions; neural; plasticity; behavior

Brain dysfunction can lead to changes in cognitive and emotional functions, and analysis of the changes and the mechanisms underlying them can lead to new insight into the ways the brain encodes learning, memory, and emotion.  The focus of this proposal is the changes in behavior that occur when the development of epileptic activity is induced by discrete electrical stimulation of regions of the rat brain, a phenomenon referred to as kindling.  My colleagues and I have demonstrated that specific  behavioral changes are associated with kindling of particular sites.  Hence behavioral change must be associated with changes in the brain structure stimulated, and not with any widespread changes that occur following seizures.  I propose to begin to identify the mechanisms of behavioral change following kindling.  I will investigate a number of potential mechanisms, at several different and inter-related levels of analysis.  Molecular:  Changes in genes and in the proteins whose synthesis is regulated by genes will be assessed after kindling of brain sites that have different behavioral consequences, with the goal of identifying changes specific to a particular site that might be related to the effects on behavior of kindling that site.  Cellular/morphological:  Similarly, I will examine the effects of kindling different sites on death or birth of nerve cells in the hippocampus, a region known to show dynamic changes in cellular existence.  Electrophysiological:  I will determine whether kindling of various sites differentially affects other forms of neural plasticity, including the responsiveness of hippocampal neurons to the rat's position in space.  Systems and circuits:  I predict that kindling of sites close to the motor/behavioral substrates of convulsions will show less plasticity than more distant sites, and I will test the prediction.  Collectively these studies should identify potential mechanisms underlying epilepsy-induced disruption of learning and memory and thereby clarify the functions of brain regions normally participating in these cognitive activities.

脑功能障碍可导致认知和情感功能的变化，对这些变化及其机制的分析可以使我们对大脑编码学习、记忆和情感的方式有新的认识。本提案的重点是当癫痫活动的发展由对大鼠大脑区域的离散电刺激引起时，一种被称为点燃的现象。我和我的同事已经证明，特定的行为变化与特定部位的点燃有关。因此，行为变化必须与刺激的大脑结构变化有关，我建议开始确定点燃后行为改变的机制。我将调查一些潜在的机制，在几个不同的和相互关联的分析水平。分子：基因和蛋白质的变化，其合成是由基因调节的，将在点燃后的大脑部位，具有不同的行为后果进行评估，以确定特定的变化，可能与点燃该网站的行为的影响特定的网站的目标。细胞/形态：同样，我将研究点燃不同部位对海马神经细胞死亡或新生的影响，海马是一个已知的显示细胞存在动态变化的区域。电生理学：我将确定不同部位的点燃是否不同地影响其他形式的神经可塑性，包括海马神经元对大鼠空间位置的反应。系统和回路：我预测，点燃的网站接近的运动/行为基板的惊厥将显示较远的网站比更少的可塑性，我将测试prediction. Collectively这些研究应该确定潜在的机制癫痫诱导的学习和记忆的中断，从而澄清通常参与这些认知活动的大脑区域的功能。