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Kim, Doyoun
시냅스 뇌질환 연구단
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Early postnatal serotonin modulation prevents adult-stage deficits in Arid1b-deficient mice through synaptic transcriptional reprogramming

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Title
Early postnatal serotonin modulation prevents adult-stage deficits in Arid1b-deficient mice through synaptic transcriptional reprogramming
Author(s)
Kim, Hyosang; Doyoun Kim; Cho, Yisul; Kyungdeok Kim; Junyeop Daniel Roh; Kim, Yangsik; Yang, Esther; Kim, Seong Soon; Ahn, Sunjoo; Kim, Hyun; Kang, Hyojin; Bae, Yongchul; Eunjoon Kim
Publication Date
2022-08
Journal
NATURE COMMUNICATIONS, v.13, no.1
Publisher
NATURE PORTFOLIO
Abstract
ARID1B is a chromatin remodeler associated with autism spectrum disorders. Here the authors demonstrate that early postnatal serotonin modulation prevents adult stage deficits in Arid1b-deficient mice through synaptic transcriptional reprogramming. Autism spectrum disorder is characterized by early postnatal symptoms, although little is known about the mechanistic deviations that produce them and whether correcting them has long-lasting preventive effects on adult-stage deficits. ARID1B, a chromatin remodeler implicated in neurodevelopmental disorders, including autism spectrum disorder, exhibits strong embryonic- and early postnatal-stage expression. We report here that Arid1b-happloinsufficient (Arid1b(+/-)) mice display autistic-like behaviors at juvenile and adult stages accompanied by persistent decreases in excitatory synaptic density and transmission. Chronic treatment of Arid1b(+/-) mice with fluoxetine, a selective serotonin-reuptake inhibitor, during the first three postnatal weeks prevents synaptic and behavioral deficits in adults. Mechanistically, these rescues accompany transcriptomic changes, including upregulation of FMRP targets and normalization of HDAC4/MEF2A-related transcriptional regulation of the synaptic proteins, SynGAP1 and Arc. These results suggest that chronic modulation of serotonergic receptors during critical early postnatal periods prevents synaptic and behavioral deficits in adult Arid1b(+/-) mice through transcriptional reprogramming.
URI
https://pr.ibs.re.kr/handle/8788114/12334
DOI
10.1038/s41467-022-32748-5
ISSN
2041-1723
Appears in Collections:
Center for Synaptic Brain Dysfunctions(시냅스 뇌질환 연구단) > 1. Journal Papers (저널논문)
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