《生命科学》 2020, 32(1): 77-82
摘 要:摘 要:孤独症是一种儿童神经发育障碍性疾病,主要症状表现为社会交往障碍及刻板重复的兴趣和行为。研究认为,环境因素和遗传因素在神经系统发育的关键时期相互作用,影响神经发生以及神经环路的连接等神经可塑性过程,引起脑内结构和功能的变化,是孤独症发病的主要原因。啮齿类动物孕期丙戊酸(VPA)暴露模型是目前被广泛认可的环境因素诱导的孤独症动物模型。现综述VPA 诱导的啮齿类动物孤独症模型脑组织形态功能变化的研究进展,并展望可能的神经环路机制。
Abstract: Abstract: Autism spectrum disorder (ASD) is a complex neurodevelopmental disorder characterized by the impairment in social interaction and communication, restricted interests, and repetitive stereotyped behaviors. Environmental factors interacting with genetic factors during prenatal and early postnatal period can influence the processes of neurogenesis and neural plasticity, which may result in autism-like behaviors. Rodent embryonic exposure to valproic acid (VPA) is a common environmental-triggered autism model. In this review, we summarize the structural and functional changes, and also discuss the prospect of neural circuits in VPA induced models of autism.