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: 8122728
• 负责人: Kathryn Amy Cross
• 金额: $ 3.27万
• 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/8122728
• 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. PUBLIC HEALTH RELEVANCE: Deficits in social abilities and imitation are seen in psychiatric conditions such as autism spectrum disorder. Recent work suggests that these impairments may result from decreased activity in a specialized neural system that is important for both the observation of actions and the execution of actions. Understanding how other brain areas control this specialized "mirror neuron system" through the study of imitation control will contribute to our understanding of the social and imitative deficits that are fundamental to these disorders.

描述（由申请人提供）：模仿经常自动和无意识地发生，特别是在社会交往中。模仿被认为依赖于一个专门的神经系统，该系统包含对动作观察和动作执行做出反应的神经元。这些所谓的镜像神经元提供了一种简约的机制，通过专门调节动作的初级运动表征的兴奋性，将关于动作的视觉信息转化为产生相同动作所必需的运动表征。这个模型能够解释自动模仿的倾向，但不清楚这种自动倾向是如何控制的，以防止永久的模仿。目前的建议的目标是阐明控制自动模仿倾向的神经机制。鉴于神经和精神病患者的模仿控制缺陷，以及早期的研究表明，一个独特的抑制机制，控制模仿，我们预测，控制模仿发生通过一个专门的控制网络，它可能涉及镜像神经元系统的调制。 模仿障碍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的行为和情绪中的作用，最近的研究已经研究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的人类镜像神经元系统的活动可能会减少。然而，这种活动减少的病因尚未探讨。两种可能性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。了解典型受试者的模仿控制，将为自闭症研究铺平道路，这些研究可以解开这两种可能性，并深入了解模仿缺陷的神经基础。 在目标1中，计划进行两项功能性磁共振成像研究，以比较直接抑制模仿与更好地理解抑制机制。模仿的控制将与反应抑制进行比较，通过停止信号范式来测量。此外，模仿控制和分辨率的空间兼容性任务中的干扰将进行比较，因为干扰分辨率一直认为依赖于不同的认知控制过程。在目标2中，将使用经颅磁刺激来评估通常研究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的模仿控制的理解，将为探索自闭症谱系障碍等精神疾病中的模仿缺陷和镜像神经元系统提供一个平台。 公共卫生相关性：社交能力和模仿能力的缺陷见于自闭症谱系障碍等精神疾病。最近的研究表明，这些损伤可能是由于一个专门的神经系统活动减少造成的，这个神经系统对观察动作和执行动作都很重要。通过对模仿控制的研究，了解其他大脑区域是如何控制这种专门的“镜像神经元系统”的，将有助于我们理解这些疾病的根本原因是社会和模仿缺陷。