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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：
8221150
负责人：
MICHAEL L PLATT
金额：
$ 31.01万
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 2016-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/8221150
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 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.

尽管行为有广泛的表型差异，但自闭症谱系障碍(ASD)患者在社交方面有共同的核心缺陷。在这里，我们认为自闭症患者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。观察他人的所作所为极大地塑造了人类的正常学习和行为。这种与他人有关的结果可以驱动观察性学习，并激发合作和嫉妒等行为。与替代奖赏相关的共情反应在个体发育早期就出现了，它们在ASD等神经精神障碍中的损害可能会产生毁灭性的后果。通过发现和操纵从他人身上发生的事情获得替代奖惩的神经机制，将促进对自闭症患者社交功能障碍的理解和治疗。尽管脑成像研究揭示了一些调节社会互动的神经回路，但替代奖赏背后的神经机制仍不清楚。我们将使用我们的新的替代奖赏行为模型来确定潜在的神经机制，描绘由于ACC或OFC可逆性失活导致的网络功能障碍对替代奖赏和其他有关行为的影响，并确定催产素(OT)对行为和神经功能的影响，催产素(OT)是一种潜在的ASD治疗干预措施。