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Fetal blockade of nicotinic acetylcholine transmission causes autism-like impairment of biological motion preference in the neonatal chick
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| Title: | Fetal blockade of nicotinic acetylcholine transmission causes autism-like impairment of biological motion preference in the neonatal chick |
| Authors: | Matsushima, Toshiya Browse this author →KAKEN DB | | Miura, Momoko Browse this author | | Patzke, Nina Browse this author | | Toji, Noriyuki Browse this author →KAKEN DB | | Wada, Kazuhiro Browse this author →KAKEN DB | | Ogura, Yukiko Browse this author →KAKEN DB | | Homma, Koichi J Browse this author | | Sgadò, Paola Browse this author | | Vallortigara, Giorgio Browse this author |
| Keywords: | autism spectrum disorder | | biological motion | | imprinting | | neonicotinoid | | valproic acid |
| Issue Date: | 18-Nov-2022 |
| Publisher: | Oxford University Press |
| Journal Title: | Cerebral Cortex Communications |
| Volume: | 3 |
| Issue: | 4 |
| Start Page: | tgac041 |
| Publisher DOI: | 10.1093/texcom/tgac041 |
| Abstract: | Several environmental chemicals are suspected risk factors for autism spectrum disorder (ASD), including valproic acid (VPA) and pesticides acting on nicotinic acetylcholine receptors (nAChRs), if administered during pregnancy. However, their target processes in fetal neuro-development are unknown. We report that the injection of VPA into the fetus impaired imprinting to an artificial object in neonatal chicks, while a predisposed preference for biological motion (BM) remained intact. Blockade of nAChRs acted oppositely, sparing imprinting and impairing BM preference. Beside ketamine and tubocurarine, significant effects of imidacloprid (a neonicotinoid insecticide) appeared at a dose ≤1 ppm. In accord with the behavioral dissociations, VPA enhanced histone acetylation in the primary cell culture of fetal telencephalon, whereas ketamine did not. VPA reduced the brain weight and the ratio of NeuN-positive cells (matured neurons) in the telencephalon of hatchlings, whereas ketamine/tubocurarine did not. Despite the distinct underlying mechanisms, both VPA and nAChR blockade similarly impaired imprinting to biological image composed of point-light animations. Furthermore, both impairments were abolished by postnatal bumetanide treatment, suggesting a common pathology underlying the social attachment malformation. Neurotransmission via nAChR is thus critical for the early social bond formation, which is hindered by ambient neonicotinoids through impaired visual predispositions for animate objects. |
| Rights: | https://creativecommons.org/licenses/by/4.0/ |
| Type: | article |
| URI: | http://hdl.handle.net/2115/87307 |
| Appears in Collections: | 理学院・理学研究院 (Graduate School of Science / Faculty of Science) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)
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Submitter: 松島 俊也
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