Impaired Epigenesis of Imprinting Predispositions Causes Autism-like Behavioral Phenotypes in Domestic Chicks

Abstract

Several environmental chemicals are suspected as risk factors for autism spectrum disorder (ASD), including valproic acid (VPA) and pesticides acting on nicotinic acetylcholine receptor (nAChR) if exposed during pregnancy. However, their target processes in fetal neuro-development are unspecified. We report that fetal injection of VPA impaired the imprinting of an artifact object in hatchlings, while the predisposed preference to biological motion (BM) remained intact. Blockade of nAChR acted oppositely, namely, spared imprinting and impaired BM in chicks. Beside ketamine and tubocurarine, significant effects of imidacloprid (a neonicotinoid insecticide) appeared at dose [≤]1ppm. Despite the distinct processes, both VPA and nAChR blockade similarly impaired imprinting of biological image composed of point-light animation. Furthermore, both impairments were rescued by post-natal bumetanide treatment, suggesting common pathology underlying the social attachment malformation. Ambient neonicotinoid could hinder adaptive socialization through impaired development of visual perception in early neonates.