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Neuronal Basis of Vicarious Reinforcement Dysfunction in Autism Spectrum Disorder

自闭症谱系障碍替代强化功能障碍的神经元基础

基本信息

批准号：
8777977
负责人：
MICHAEL L PLATT
金额：
$ 30.96万
依托单位：
DUKE UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2012
资助国家：
美国
起止时间：
2012-02-21 至 2015-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8777977
关键词：
Animal Model Anterior Attention Behavior Behavioral Model Brain Brain imaging Caring Cervical Code Computers Cues Data Disease Electric Stimulation Ethics Functional disorder Growth Human Impairment Individual Investigation Learning Lesion Macaca mulatta Measures Mediating Modeling Monkeys National Institute of Mental Health Neurons Neurophysiology - biologic function Operant Conditioning Outcome Oxytocin Pattern Penetration Process Psychological reinforcement Puncture procedure Punishment Reaction Time Reference Values Rewards Saline Shapes Signal Transduction Social Interaction Techniques Testing Therapeutic Intervention Variant Visual Work autism spectrum disorder base cingulate cortex classical conditioning electrical microstimulation experience gaze improved insight learned behavior microstimulation motivated behavior network dysfunction neural circuit neuromechanism neurophysiology neuropsychiatry preference response social

项目摘要

Despite a broad continuum of phenotypic variation in behavior, individuals with autism spectrum disorders (ASD) share core deficits in social interaction. Here we propose that social dysfunction in ASD results, in part, from impairments in deriving vicarious reinforcement from others. Observing what happens to others powerfully shapes normal human learning and behavior. Such other-regarding outcomes can drive observational learning, and motivate behaviors such as cooperation, as well as envy. Empathic responses associated with vicarious reward appear early in ontogeny, and their impairment in neuropsychiatric disorders like ASD can have devastating consequences. Understanding and treating social dysfunction in ASD will be advanced by discovering and manipulating the neural mechanisms that derive vicarious reward and punishment from what happens to others. Although brain-imaging studies have revealed some of the neural circuitry mediating social interactions, the neuronal mechanisms underlying vicarious reward remain unknown. We will use our new behavioral model of vicarious reward to determine the underlying neuronal mechanisms, delineate the impacts of network dysfunction due to reversible inactivation of ACC or OFC on vicarious reward and other-regarding behavior, and define the effects of oxytocin (OT), a potential therapeutic intervention for ASD, on behavior and neural function.

尽管在行为上存在广泛的连续表型变异，但自闭症谱系障碍（ASD）患者在社会交往方面存在共同的核心缺陷。在这里，我们提出ASD的社会功能障碍部分是由于从他人那里获得替代强化的障碍。观察发生在别人身上的事情会有力地塑造人类正常的学习和行为。这种与他人相关的结果可以推动观察学习，并激发合作和嫉妒等行为。与替代奖励相关的共情反应在个体发育早期就出现了，在ASD等神经精神疾病中，它们的损害可能会造成毁灭性的后果。通过发现和操纵从他人身上发生的事情中获得替代奖励和惩罚的神经机制，将有助于理解和治疗ASD中的社会功能障碍。尽管脑成像研究已经揭示了一些调节社会互动的神经回路，但替代奖励背后的神经机制仍然未知。我们将使用我们新的替代奖励行为模型来确定潜在的神经元机制，描述由于ACC或OFC可逆失活而导致的网络功能障碍对替代奖励和其他相关行为的影响，并定义催产素（OT）对行为和神经功能的影响，催产素是ASD的潜在治疗干预措施。