Neural mechanisms of imitative behavior: Implications for mental health

描述(由申请人提供)：模仿通常是自动的和无意识的，特别是在社交互动中。模仿被认为依赖于一种特殊的神经系统，该神经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，通过特定地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。这个模型能够解释模仿的自动倾向，但目前还不清楚这种自动倾向是如何控制的，以防止永久模仿。目前这项提议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明显的抑制机制，我们预测模仿的控制通过一个专门的控制网络发生，它可能涉及到镜像神经元系统的调节。模仿障碍是自闭症谱系障碍的一个特征。由于镜像神经元在理解他人行为和情绪中的作用，最近的研究已经研究了镜像神经元在自闭症中的功能。越来越多的证据表明，与典型的发育中的儿童相比，自闭症谱系障碍患者的人类镜像神经系统中的活动可能会减少。然而，这种活动减少的原因还没有被探索。两种可能性包括固有的镜像神经系统功能障碍和不同的神经回路对镜像神经系统的调节受损。了解典型受试者对模仿的控制，将为自闭症的研究铺平道路，从而将这两种可能性区分开来，并提供对模仿缺陷的神经基础的洞察。在目标1中，计划进行两项功能磁共振成像研究，以比较直接的模仿抑制和更好地理解抑制机制。模仿的控制将与反应抑制进行比较，这是通过停止信号范式衡量的。此外，还将比较空间相容任务中的模仿控制和干扰解决，因为干扰解决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。在正常人群中对基础水平上的模仿控制的更好的理解将为探索模仿的缺陷和自闭症谱系障碍等精神疾病中的镜像神经系统提供一个平台。

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.