[논문]A DLG2 deficiency in mice leads to reduced sociability and increased repetitive behavior accompanied by aberrant synaptic transmission in the dorsal striatum

Yoo, Taesun; Kim, Sun-Gyun; Yang, Soo Hyun; Kim, Hyun; Kim, Eunjoon; Kim, Soo Young

doi:10.1186/s13229-020-00324-7

[해외논문] A DLG2 deficiency in mice leads to reduced sociability and increased repetitive behavior accompanied by aberrant synaptic transmission in the dorsal striatum 원문보기

Molecular autism, v.11 no.1, 2020년, pp.19 -

Yoo, Taesun (Department of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141 Korea) , Kim, Sun-Gyun (Center for Synaptic Brain Dysfunctions, Institute for Basic Science (IBS), Daejeon, 34141 Korea) , Yang, Soo Hyun (Department of Anatomy, College of Medicine, Korea University, Seoul, 02841 Korea) , Kim, Hyun (Department of Anatomy, College of Medicine, Korea University, Seoul, 02841 Korea) , Kim, Eunjoon (Department of Biological Sciences, Korea Advanced Institute for Science and Technology (KAIST), Daejeon, 34141 Korea) , Kim, Soo Young (College of Pharmacy, Yeungnam University, Gyeongsan, 38541 Korea)

Abstract ▼ AI-Helper

BackgroundDLG2, also known as postsynaptic density protein-93 (PSD-93) or chapsyn-110, is an excitatory postsynaptic scaffolding protein that interacts with synaptic surface receptors and signaling molecules. A recent study has demonstrated that mutations in the DLG2 promoter region are significantly associated with autism spectrum disorder (ASD). Although DLG2 is well known as a schizophrenia-susceptibility gene, the mechanisms that link DLG2 gene disruption with ASD-like behaviors remain unclear.MethodsMice lacking exon 14 of the Dlg2 gene (Dlg2–/– mice) were used to investigate whether Dlg2 deletion leads to ASD-like behavioral abnormalities. To this end, we performed a battery of behavioral tests assessing locomotion, anxiety, sociability, and repetitive behaviors. In situ hybridization was performed to determine expression levels of Dlg2 mRNA in different mouse brain regions during embryonic and postnatal brain development. We also measured excitatory and inhibitory synaptic currents to determine the impacts of Dlg2 deletion on synaptic transmission in the dorsolateral striatum.ResultsDlg2–/– mice showed hypoactivity in a novel environment. They also exhibited decreased social approach, but normal social novelty recognition, compared with wild-type animals. In addition, Dlg2–/– mice displayed strong self-grooming, both in home cages and novel environments. Dlg2 mRNA levels in the striatum were heightened until postnatal day 7 in mice, implying potential roles of DLG2 in the development of striatal connectivity. In addition, the frequency of excitatory, but not inhibitory, spontaneous postsynaptic currents in the Dlg2–/– dorsolateral striatum was significantly reduced.ConclusionThese results suggest that homozygous Dlg2 deletion in mice leads to ASD-like behavioral phenotypes, including social deficits and increased repetitive behaviors, as well as reductions in excitatory synaptic input onto dorsolateral spiny projection neurons, implying that the dorsal striatum is one of the brain regions vulnerable to the developmental dysregulation of DLG2.

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