Abnormalities of the serotonergic system in diacylglycerol kinase δ-deficient mouse brain

Qiang Lu, Suguru Komenoi, Takako Usuki, Daisuke Takahashi, Fumio Sakane

研究成果: ジャーナルへの寄稿記事

抄録

We previously reported that brain-specific diacylglycerol kinase (DGK) δ-knockout (KO) mice showed obsessive-compulsive disorder (OCD)-like behaviors, which were alleviated by a serotonin (5-HT) transporter (SERT) inhibitor. However, the molecular mechanisms causing the OCD-like abnormal behaviors remain unclear. In the present study, we found that DGKδ deficiency increased SERT protein levels in the mouse cerebral cortex. Moreover, DGKδ interacted and co-localized with SERT. Furthermore, DGKδ-KO decreased tryptophan hydroxylase-2 expression and increased monoamine oxidase-A expression. Indeed, the amount of 5-HT in the cerebral cortex was significantly decreased in DGKδ-KO mice. These data strongly suggest that OCD-like behaviors in the DGKδ-KO mice are caused by comprehensive and composite serotonergic hypofunction.

元の言語英語
ページ(範囲)1031-1037
ページ数7
ジャーナルBiochemical and Biophysical Research Communications
497
発行部数4
DOI
出版物ステータス出版済み - 3 18 2018

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Diacylglycerol Kinase
Brain
Obsessive-Compulsive Disorder
Knockout Mice
Serotonin
Cerebral Cortex
EphA5 Receptor
Tryptophan Hydroxylase
Serotonin Plasma Membrane Transport Proteins
Monoamine Oxidase
Composite materials

これを引用

Abnormalities of the serotonergic system in diacylglycerol kinase δ-deficient mouse brain. / Lu, Qiang; Komenoi, Suguru; Usuki, Takako; Takahashi, Daisuke; Sakane, Fumio.

:: Biochemical and Biophysical Research Communications, 巻 497, 番号 4, 18.03.2018, p. 1031-1037.

研究成果: ジャーナルへの寄稿記事

Lu, Qiang ; Komenoi, Suguru ; Usuki, Takako ; Takahashi, Daisuke ; Sakane, Fumio. / Abnormalities of the serotonergic system in diacylglycerol kinase δ-deficient mouse brain. :: Biochemical and Biophysical Research Communications. 2018 ; 巻 497, 番号 4. pp. 1031-1037.
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abstract = "We previously reported that brain-specific diacylglycerol kinase (DGK) δ-knockout (KO) mice showed obsessive-compulsive disorder (OCD)-like behaviors, which were alleviated by a serotonin (5-HT) transporter (SERT) inhibitor. However, the molecular mechanisms causing the OCD-like abnormal behaviors remain unclear. In the present study, we found that DGKδ deficiency increased SERT protein levels in the mouse cerebral cortex. Moreover, DGKδ interacted and co-localized with SERT. Furthermore, DGKδ-KO decreased tryptophan hydroxylase-2 expression and increased monoamine oxidase-A expression. Indeed, the amount of 5-HT in the cerebral cortex was significantly decreased in DGKδ-KO mice. These data strongly suggest that OCD-like behaviors in the DGKδ-KO mice are caused by comprehensive and composite serotonergic hypofunction.",
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AU - Lu, Qiang

AU - Komenoi, Suguru

AU - Usuki, Takako

AU - Takahashi, Daisuke

AU - Sakane, Fumio

N1 - Copyright © 2018 Elsevier Inc. All rights reserved.

PY - 2018/3/18

Y1 - 2018/3/18

N2 - We previously reported that brain-specific diacylglycerol kinase (DGK) δ-knockout (KO) mice showed obsessive-compulsive disorder (OCD)-like behaviors, which were alleviated by a serotonin (5-HT) transporter (SERT) inhibitor. However, the molecular mechanisms causing the OCD-like abnormal behaviors remain unclear. In the present study, we found that DGKδ deficiency increased SERT protein levels in the mouse cerebral cortex. Moreover, DGKδ interacted and co-localized with SERT. Furthermore, DGKδ-KO decreased tryptophan hydroxylase-2 expression and increased monoamine oxidase-A expression. Indeed, the amount of 5-HT in the cerebral cortex was significantly decreased in DGKδ-KO mice. These data strongly suggest that OCD-like behaviors in the DGKδ-KO mice are caused by comprehensive and composite serotonergic hypofunction.

AB - We previously reported that brain-specific diacylglycerol kinase (DGK) δ-knockout (KO) mice showed obsessive-compulsive disorder (OCD)-like behaviors, which were alleviated by a serotonin (5-HT) transporter (SERT) inhibitor. However, the molecular mechanisms causing the OCD-like abnormal behaviors remain unclear. In the present study, we found that DGKδ deficiency increased SERT protein levels in the mouse cerebral cortex. Moreover, DGKδ interacted and co-localized with SERT. Furthermore, DGKδ-KO decreased tryptophan hydroxylase-2 expression and increased monoamine oxidase-A expression. Indeed, the amount of 5-HT in the cerebral cortex was significantly decreased in DGKδ-KO mice. These data strongly suggest that OCD-like behaviors in the DGKδ-KO mice are caused by comprehensive and composite serotonergic hypofunction.

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