Ergaz Zivanit, Weinstein-Fudim Liza, Ornoy Asher
Laboratory of Teratology, Department of Medical Neurobiology Hebrew University Hadassah Medical School and Hadassah Hospital, Jerusalem, Israel.
Laboratory of Teratology, Department of Medical Neurobiology Hebrew University Hadassah Medical School and Hadassah Hospital, Jerusalem, Israel.
Reprod Toxicol. 2016 Sep;64:116-40. doi: 10.1016/j.reprotox.2016.04.024. Epub 2016 Apr 30.
Autism spectrum disorder (ASD) is associated, in addition to complex genetic factors, with a variety of prenatal, perinatal and postnatal etiologies. We discuss the known animal models, mostly in mice and rats, of ASD that helps us to understand the etiology, pathogenesis and treatment of human ASD. We describe only models where behavioral testing has shown autistic like behaviors. Some genetic models mimic known human syndromes like fragile X where ASD is part of the clinical picture, and others are without defined human syndromes. Among the environmentally induced ASD models in rodents, the most common model is the one induced by valproic acid (VPA) either prenatally or early postnatally. VPA induces autism-like behaviors following single exposure during different phases of brain development, implying that the mechanism of action is via a general biological mechanism like epigenetic changes. Maternal infection and inflammation are also associated with ASD in man and animal models.
除复杂的遗传因素外，自闭症谱系障碍（ASD）还与多种产前、围产期和产后病因相关。我们讨论了已知的主要针对小鼠和大鼠的ASD动物模型，这些模型有助于我们理解人类ASD的病因、发病机制和治疗方法。我们仅描述行为测试显示出类似自闭症行为的模型。一些遗传模型模拟已知的人类综合征，如脆性X综合征，其中ASD是临床表现的一部分，而其他模型则没有明确的人类综合征。在啮齿动物中由环境诱导的ASD模型中，最常见的模型是产前或产后早期由丙戊酸（VPA）诱导的模型。VPA在大脑发育的不同阶段单次暴露后会诱发类似自闭症的行为，这意味着其作用机制是通过一种普遍的生物学机制，如表观遗传变化。母体感染和炎症在人类和动物模型中也与ASD有关。
