Basal Ganglia - Cortical Interactions in Motor Control

基底神经节 - 运动控制中的皮质相互作用

• 批准号: 6979755
• 负责人: JONATHAN W. MINK
• 金额: $ 21.43万
• 依托单位: UNIVERSITY OF ROCHESTER
• 依托单位国家: 美国
• 财政年份: 2005
• 资助国家: 美国
• 起止时间: 2005-04-01 至 2010-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6979755
• 关键词: Macaca mulatta; autonomic reflex; basal ganglia; behavior test; behavioral /social science research tag; cell cell interaction; lenticular nucleus; limb movement; motor cortex; neural information processing; neural inhibition; neuromuscular disorder; psychomotor function; thalamocortical tract

The basal ganglia are important components of the motor system. Diseases of the basal ganglia cause impaired voluntary movement, abnormal involuntary movements, or both. It is generally agreed that the basal ganglia function in concert with cerebral cortical mechanisms in the control of many aspects of behavior. A large portion of the basal ganglia-thalmocortical circuitry is devoted to the control of movement. Despite substantial advances in understanding the contributions of these circuits to motor control, there is still no consensus as to how the basal ganglia output influences cortical motor areas. The proposed experiments will investigate the function of basal ganglia-thalamocortical circuits in the control of limb movement in primates. Selective inactivation of basal ganglia output neurons in globus pallidus, pars interna (GPi) will be combined with recording neuronal activity in cortical targets of that output while monkeys perform a wrist movement task. We have hypothesized that a key function of the basal ganglia in voluntary movement is to facilitate the desired motor pattern and to simultaneously inhibit potentially competing motor patterns so that they do not interfere with the one that has been selected. We will test this overall hypothesis in 2 specific aims. We will determine how movement-related neuronal signals in supplementary motor area (SMA) and primary motor cortex (MC) change after reversible inactivation of GPi and how those signal changes relate to the resulting motor impairment. We will also determine if GPi activity correlates with suppression of an "automatic" movement response and whether inactivation of GPi prevents suppression of that response and interferes with performance of a movement in the opposite direction from the "automatic" response. These experiments will directly test the effect on cortical motor physiology of inactivating the basal gangia output for limb movements. They will provide important new information on how the basal ganglia interact with motor areas of cerebral cortex. This results of this project will enhance understanding of normal basal ganglia function in motor control and will provide important clues to the pathophysiology of movement disorders resulting from basal ganglia diseases. Better understanding of these mechanisms will have potential significant impact on development of better therapies for those movement disorders.

基底神经节是运动系统的重要组成部分。基底神经节疾病会导致随意运动受损、不随意运动异常或两者兼而有之。人们普遍认为，基底神经节在控制行为的许多方面与大脑皮层机制协同发挥作用。基底神经节-丘脑皮质回路的很大一部分专门用于控制运动。尽管在理解这些电路对运动控制的贡献方面取得了实质性进展，但对于基底神经节输出如何影响皮质运动区域仍没有达成共识。拟议的实验将研究基底神经节-丘脑皮质回路在控制灵长类动物肢体运动中的功能。苍白球、内部基底神经节输出神经元的选择性失活 当猴子执行手腕运动任务时，（GPi）将与记录该输出的皮质目标中的神经元活动相结合。我们假设基底神经节在随意运动中的一个关键功能是促进所需的运动模式，并同时抑制潜在的竞争运动模式，以便它们不会干扰已选择的运动模式。我们将在两个具体目标中检验这一总体假设。我们将确定辅助运动区 (SMA) 和初级运动区中运动相关的神经元信号如何 GPi 可逆失活后皮质 (MC) 的变化以及这些信号变化与由此产生的运动障碍的关系。我们还将确定 GPi 活动是否与“自动”运动响应的抑制相关，以及 GPi 失活是否会阻止对该响应的抑制并干扰与“自动”响应相反方向的运动性能。这些实验将直接测试使肢体运动的基底神经节输出失活对皮质运动生理学的影响。他们将提供有关基底神经节如何与大脑皮层运动区相互作用的重要新信息。该项目的结果将增强对运动控制中正常基底神经节功能的理解，并将为基底神经节疾病引起的运动障碍的病理生理学提供重要线索。更好地了解这些机制将对开发更好的运动障碍疗法产生潜在的重大影响。