Neural mechanisms of imitative behavior: Implications for mental health

模仿行为的神经机制：对心理健康的影响

• 批准号: 8411391
• 负责人: Kathryn Amy Cross
• 金额: $ 3.31万
• 依托单位: UNIVERSITY OF CALIFORNIA LOS ANGELES
• 依托单位国家: 美国
• 财政年份: 2011
• 资助国家: 美国
• 起止时间: 2011-08-01 至 2014-07-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8411391
• 关键词: Area; Autistic Disorder; Behavior; Brain; Brain region; Child; Communication; Conscious; Controlled Study; Corpus striatum structure; Defect; Disease; Dissociation; Echolalia; Emotions; Empathy; Etiology; Fire - disasters; Functional Magnetic Resonance Imaging; Functional disorder; Goals; Human; Imitative Behavior; Impairment; Intervention; Investigation; Lead; Light; Maps; Measures; Mental Health; Modeling; Monkeys; Motor; Neurologic; Neurons; Patients; Performance; Persons; Population; Process; Regulation; Reliance; Reporting; Research; Resolution; Response to stimulus physiology; Role; Scientist; Severities; Signal Transduction; Simulate; Social Interaction; Symptoms; System; Transcranial magnetic stimulation; Translating; Unconscious State; Visual; Work; autism spectrum disorder; base; cognitive control; improved; insight; mirror neuron; mirror neuron system; motor control; neural circuit; neuromechanism; prevent; psychologic; relating to nervous system; repetitive transcranial magnetic stimulation; research study; response; simulation; social; visual information

DESCRIPTION (provided by applicant): Imitation often occurs automatically and unconsciously, especially during social interactions. Imitation is thought to rely on a specialized neural system that contains neurons responsive to both action observation and action execution. These so-called mirror neurons provide a parsimonious mechanism to translate visual information about an action into the motor representation necessary to produce the same action, by specifically modulating the excitability of the primary motor representation of the action. This model is able to explain the automatic tendency to imitate, however it is not clear how this automatic tendency is controlled to prevent perpetual imitation. The goal of the current proposal is to elucidate the neural mechanisms that control the automatic tendency to imitate. In light of neurological and psychiatric patients with imitation control deficits, as well as early research suggesting a distinct inhibitory mechanism for control imitation, we predict that control of imitation occurs through a specialized control network and that it may involve modulation of the mirror neuron system. Impaired imitation is a hallmark of autism spectrum disorders. Due to the proposed role of mirror neurons in understanding others' actions and emotions, recent research has examined mirror neuron function in autism. Converging evidence suggests that activity in the human mirror neuron system may be decreased in autism spectrum disorders compared to typically developing children. However, the etiology of this decrease in activity has not been explored. Two possibilities include intrinsic mirror neuron system dysfunction and impaired regulation of the mirror neuron system by distinct neural circuitry. Understanding control of imitation in typical subjects will pave the way for studies in autism that can disentangle these two possibilities as well as provide insight into the neural underpinnings of the imitative deficits. In Aim 1, two functional magnetic resonance imaging studies are planned to compare inhibition of imitation directly with better understood inhibitory mechanisms. Control of imitation will be compared with response inhibition, as measured by the stop-signal paradigm. In addition, imitation control and resolution of interference in a spatial compatibility task will be compared, since interference resolution has been argued to rely on distinct cognitive control processes. In Aim 2, transcranial magnetic stimulation will be used to evaluate the causal roles of commonly studied control mechanisms in control of imitation. Improved understanding of control of imitation at a basic level in normal populations will provide a platform to explore deficits in imitation and the mirror neuron system in psychiatric illnesses such as autism spectrum disorders.

描述（由申请人提供）：模仿经常是自动和无意识地发生的，尤其是在社会交往中。模仿被认为依赖于一个特殊的神经系统，该系统包含对动作观察和动作执行都有反应的神经元。这些所谓的镜像神经元提供了一种简约的机制，通过特定地调节动作的主要运动表征的兴奋性，将有关动作的视觉信息转化为产生相同动作所需的运动表征。这个模型能够解释模仿的自动倾向，但是不清楚这种自动倾向是如何被控制以防止永久模仿的。本研究的目标是阐明控制自动模仿倾向的神经机制。鉴于有模仿控制缺陷的神经病学和精神病学患者，以及早期研究表明控制模仿存在独特的抑制机制，我们预测模仿的控制是通过一个专门的控制网络发生的，它可能涉及镜像神经元系统的调节。模仿能力受损是自闭症谱系障碍的一个标志。由于镜像神经元在理解他人行为和情绪方面的作用被提出，最近的研究已经检查了自闭症中的镜像神经元功能。越来越多的证据表明，与正常发育的儿童相比，自闭症谱系障碍患者镜像神经元系统的活动可能会减少。然而，这种活性降低的病因尚未被探讨。两种可能包括内在镜像神经元系统功能障碍和不同神经回路对镜像神经元系统的调节受损。理解典型受试者对模仿的控制将为自闭症研究铺平道路，从而理清这两种可能性，并深入了解模仿缺陷的神经基础。在Aim 1中，两项功能性磁共振成像研究计划将模仿的抑制与更好地理解的抑制机制进行比较。模仿控制将与反应抑制进行比较，通过停止信号范式进行测量。此外，将比较空间兼容性任务中的模仿控制和干扰解决，因为干扰解决一直被认为依赖于不同的认知控制过程。在目标2中，经颅磁刺激将用于评估常见的控制机制在控制模仿中的因果作用。提高对正常人群基本水平模仿控制的理解，将为探索自闭症谱系障碍等精神疾病的模仿缺陷和镜像神经元系统提供一个平台。