Department of Psychology, Program in Neuroscience, University of Nevada, Reno, USA.
Department of Psychiatry and Behavioral Science, University of Louisville School of Medicine, Louisville, USA.
Neuropathol Appl Neurobiol. 2016 Feb;42(2):115-34. doi: 10.1111/nan.12227. Epub 2015 May 2.
The cerebral cortex undergoes protracted maturation during human development and exemplifies how biology and environment are inextricably intertwined in the construction of complex neural circuits. Autism spectrum disorders are characterized by a number of pathological changes arising from this developmental process. These include: (i) alterations to columnar structure that have significant implications for the organization of cortical circuits and connectivity; (ii) alterations to synaptic spines on individual cortical units that may underlie specific types of connectional changes; and (iii) alterations within the cortical subplate, a region that plays a role in proper cortical development and in regulating interregional communication in the mature brain. Although the cerebral cortex is not the only structure affected in the disorder, it is a fundamental contributor to the behaviours that characterize autism. These alterations to cortical circuitry likely underlie the behavioural phenotype in autism and contribute to the unique pattern of deficits and strengths that characterize cognitive functioning. Recent findings within the cortical subplate may indicate that alterations to cortical construction begin prenatally, before activity-dependent connections are established, and are in need of further study. A better understanding of cortical development in autism spectrum disorders will draw bridges between the microanatomical computational circuitry and the atypical behaviours that arise when that circuitry is modified. In addition, it will allow us to better exploit the constructional plasticity within the brain to design more targeted interventions that better manage atypical cortical construction and that can be applied very early in postnatal life.
大脑皮层在人类发育过程中经历了长时间的成熟，它例证了生物学和环境在构建复杂神经回路方面是如何不可分割地交织在一起的。自闭症谱系障碍的特征是由这一发展过程引起的许多病理变化。这些变化包括：（i）柱结构的改变，这对皮质回路和连接的组织有重大影响；（ii）单个皮质单元上的突触棘突的改变，可能是特定类型的连接变化的基础；以及（iii）皮质基板内的改变，该区域在皮质的正常发育和调节成熟大脑中的区域间通讯中发挥作用。虽然大脑皮层不是该疾病中唯一受影响的结构，但它是构成自闭症特征的行为的基本贡献者。皮质回路的这些改变可能是自闭症行为表型的基础，并导致认知功能的独特缺陷和优势模式。皮质基板内的最新发现可能表明，皮质结构的改变始于产前，即在活动依赖性连接建立之前，并需要进一步研究。更好地了解自闭症谱系障碍中的皮质发育将在微观解剖计算回路和当该回路被修改时出现的异常行为之间架起桥梁。此外，它将使我们能够更好地利用大脑的结构可塑性，设计更有针对性的干预措施，更好地管理异常的皮质结构，并可以在产后生活的早期应用。
