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논문 기본 정보

자료유형
학술저널
저자정보
Chang Bomi (Center for Cognition and Sociality Institute for Basic Science Daejeon 34126 KoreaBrain Science Ins) 변준원 (Center for Cognition and Sociality Institute for Basic Science Daejeon 34126 Korea) Kim Ko Keun (Center for Cognition and Sociality Institute for Basic Science Daejeon 34126 Korea) 이성은 (Brain Science Institute Korea Institute of Science and Technology) 이보영 (Center for Cognition and Sociality Institute for Basic Science Daejeon 34126 Korea) 김기선 (한국과학기술연구원) 류훈 (Brain Science Institute Korea Institute of Science and Technology) 신희섭 (Center for Cognition and Sociality Institute for Basic Science) 정은지 (연세대학교)
저널정보
한국뇌신경과학회 Experimental Neurobiology Experimental Neurobiology Vol.31 No.2
발행연도
2022.4
수록면
116 - 130 (15page)
DOI
10.5607/en22007

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Absence seizures are caused by abnormal synchronized oscillations in the thalamocortical (TC) circuit, which result in widespread spike-and-wave discharges (SWDs) on electroencephalography (EEG) as well as impairment of consciousness. Thalamic reticular nucleus (TRN) and TC neurons are known to interact dynamically to generate TC circuitry oscillations during SWDs. Clinical studies have suggested the association of Plcβ1 with early-onset epilepsy, including absence seizures. However, the brain regions and circuit mechanisms related to the generation of absence seizures with Plcβ1 deficiency are unknown. In this study, we found that loss of Plcβ1 in mice caused spontaneous complex-type seizures, including convulsive and absence seizures. Importantly, TRN-specific deletion of Plcβ1 led to the development of only spontaneous SWDs, and no other types of seizures were observed. Ex vivo slice patch recording demonstrated that the number of spikes, an intrinsic TRN neuronal property, was significantly reduced in both tonic and burst firing modes in the absence of Plcβ1 . We conclude that the loss of Plcβ1 in the TRN leads to decreased excitability and impairs normal inhibitory neuronal function, thereby disrupting feedforward inhibition of the TC circuitry, which is sufficient to cause hypersynchrony of the TC system and eventually leads to spontaneous absence seizures. Our study not only provides a novel mechanism for the induction of SWDs in Plcβ1 -deficient patients but also offers guidance for the development of diagnostic and therapeutic tools for absence epilepsy.

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