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M. Okada, Y. Hozumi, T. Tanaka, Y. Suzuki, M. Yanagida, Y. Araki, C. Evangelisti, H. Yagisawa, M. K. Topham, A. M. Martelli and K. Goto, “DGKzeta Is Degraded through the Cytoplasmic Ubiquitin-Proteasome System under Excitotoxic Conditions, Which Causes Neuronal Apoptosis Because of Aberrant Cell Cycle Reentry,” Cell Signalling, Vol. 24, No. 8, 2012, pp. 1573-1582. doi:10.1016/j.cellsig.2012.03.021

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• TITLE: Increased Seizure Susceptibility in a Mouse with Diacylglycerol Kinase β Deficiency

  AUTHORS: Mitsue Ishisaka, Kazuhiro Tsuruma, Masamitsu Shimazawa, Yasuhito Shirai, Naoaki Saito, Hideaki Hara

  KEYWORDS: Diacylglycerol Kinase; Seizure; Parvalbumin

  JOURNAL NAME: Neuroscience and Medicine, Vol.4 No.2, June 18, 2013

  ABSTRACT: Diacylglycerol kinase (DGK) is an enzyme that converts diacylglycerol to phosphatidic acid. Several DGK isoforms have been implicated in the pathogenesis of seizure, but the role of DGKβ in seizure is unknown. In the present study, we investigated the involvement of DGKβ in seizure using DGKβ knockout (KO) mice. Seizures were more severe in DGKβ KO mice than in wild-type (WT) mice after pentylenetetrazol (PTZ) treatment and after kainic acid treatment, but there were no differences in latency to seizure. The expression levels of DGKβ in the hippocampal CA1, CA3, or DG areas did not differ between PTZ (60 mg/kg) treatment and saline treatment. There were fewer parvalbumin-positive interneurons in the hippocampal CA3 area in DGKβ KO mice than in control WT mice, which might partly account for the increased seizure susceptibility displayed by DGKβ KO mice. These results suggest that DGKβ may play a pivotal role in the development of the relevant interneurons, and that on inherent deficiency of DGKβ increases the animal’s sensitivity to seizure-inducing stimuli.