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.