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自闭症患者社会功能的神经生物学相关性。

Neurobiological correlates of social functioning in autism.

机构信息

Department of Psychology, University of Washington, Box 351525, Seattle, WA 98195-1525, USA.

出版信息

Clin Psychol Rev. 2010 Aug;30(6):733-48. doi: 10.1016/j.cpr.2010.05.007. Epub 2010 May 27.

Abstract

Although autism is defined by deficits in three areas of functioning (social, communicative, and behavioral), impairments in social interest and restricted behavioral repertoires are central to the disorder. As a result, a detailed understanding of the neurobiological systems subserving social behavior may have implications for prevention, early identification, and intervention for affected families. In this paper, we review a number of potential neurobiological mechanisms--across several levels of analysis--that subserve normative social functioning. These include neural networks, neurotransmitters, and hormone systems. After describing the typical functioning of each system, we review available empirical findings specific to autism. Among the most promising potential mechanisms of social behavioral deficits in autism are those involving neural networks including the amygdala, the mesocorticolimbic dopamine system, and the oxytocin system. Particularly compelling are explanatory models that integrate mechanisms across biological systems, such as those linking dopamine and oxytocin with brain regions critical to reward processing.

摘要

尽管自闭症的定义是在三个功能领域(社交、沟通和行为)存在缺陷,但社交兴趣和受限的行为范围的损伤是该疾病的核心。因此,对支持社交行为的神经生物学系统的详细了解可能对受影响家庭的预防、早期识别和干预具有重要意义。在本文中,我们回顾了一些潜在的神经生物学机制——跨越多个分析层次——这些机制支持正常的社交功能。这些包括神经网络、神经递质和激素系统。在描述了每个系统的典型功能后,我们回顾了与自闭症相关的现有实证发现。在自闭症的社交行为缺陷的最有希望的潜在机制中,有涉及神经网络的机制,包括杏仁核、中脑边缘多巴胺系统和催产素系统。特别引人注目的是那些整合跨生物系统机制的解释模型,例如将多巴胺和催产素与对奖励处理至关重要的大脑区域联系起来的模型。

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