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This galley proof is being listed electronically before publishing the final manuscript (It's not final version).

Autistic-like social deficits in hippocampal MeCP2 knockdown rat models are rescued by ketamine
Miyeon Choi1,# (Postdoctoral researcher), Seung Yeon Ko1,# (Postdoctoral researcher), Jee Young Seo2 (Graduate student), Do Gyeong Kim2 (Graduate student), Huiju Lee2 (Graduate student), Heekyoung Chung2 (Professor), Hyeon Son 2,3,* (Professor)
1Hanyang Biomedical Research Institute and 2Graduate School of Biomedical Science and Engineering, Hanyang University,
3Department of Biochemistry and Molecular Biology, College of Medicine, Hanyang University
Autism or autism spectrum disorder (ASD) is a behavioral syndrome characterized by persistent deficits in social interaction, and repetitive patterns of behavior, interests, or activities. The gene encoding Methyl-CpG binding protein 2 (MeCP2) is one of a few exceptional genes of established causal effect in ASD. Although genetically engineered mice studies may shed light on how MeCP2 loss affects synaptic activity patterns across the whole brain, such studies are not considered practical in ASD patients due to the overall level of impairment, and are technically challenging in mice. For the first time, we show that hippocampal MeCP2 knockdown produces behavioral abnormalities associated with autism-like traits in rats, providing a new strategy to investigate the efficacy of therapeutics in ASD. Ketamine, an N-Methyl-D-aspartate (NMDA) blocker, has been proposed as a possible treatment for autism. Using the MeCP2 knockdown rats in conjunction with a rat model of valproic acid (VPA)-induced ASD, we examined gene expression and ASD behaviors upon ketamine treatment. We report that the core symptoms of autism in MeCP2 knockdown rats with social impairment recovered dramatically following a single treatment with ketamine.
Abstract, Accepted Manuscript(in press) [Submitted on February 24, 2022, Accepted on March 18, 2022]
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