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Overexpression of transmembrane protein 168 in the mouse nucleus accumbens induces anxiety and sensorimotor gating deficit
http://hdl.handle.net/10110/00018215
http://hdl.handle.net/10110/0001821575a9ec7c-7c8e-4235-b411-033872518ca3
Item type | 学術雑誌論文 / Journal Article(1) | |||||
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公開日 | 2018-02-25 | |||||
タイトル | ||||||
タイトル | Overexpression of transmembrane protein 168 in the mouse nucleus accumbens induces anxiety and sensorimotor gating deficit | |||||
言語 | ||||||
言語 | eng | |||||
資源タイプ | ||||||
資源タイプ識別子 | http://purl.org/coar/resource_type/c_6501 | |||||
資源タイプ | journal article | |||||
著者 |
Fu, Kequan
× Fu, Kequan× Miyamoto, Yoshiaki× Sumi, Kazuyuki× Saika, Eriko× Muramatsu, Shin-ichi× Uno, Kyosuke× Nitta, Atsumi |
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抄録 | ||||||
内容記述タイプ | Abstract | |||||
内容記述 | Transmembrane protein 168 (TMEM168) comprises 697 amino acid residues, including some putative transmembrane domains. It is reported that TMEM168 controls methamphetamine (METH) dependence in the nucleus accumbens (NAc) of mice. Moreover, a strong link between METH dependence-induced adaptive changes in the brain and mood disorders has been evaluated. In the present study, we investigated the effects of accumbal TMEM168 in a battery of behavioral paradigms. The adeno-associated virus (AAV) Tmem168 vector was injected into the NAc of C57BL/6J mice (NAc-TMEM mice). Subsequently, the accumbal TMEM168 mRNA was increased approximately by seven-fold when compared with the NAc-Mock mice (controls). The NAc-TMEM mice reported no change in the locomotor activity, cognitive ability, social interaction, and depression-like behaviors; however, TMEM168 overexpression enhanced anxiety in the elevated-plus maze and light/dark box test. The increased anxiety was reversed by pretreatment with the antianxiety drug diazepam (0.3 mg/kg i.p.). Moreover, the NAc-TMEM mice exhibited decreased prepulse inhibition (PPI) in the startle response test, and the induced schizophrenia-like behavior was reversed by pretreatment with the antipsychotic drug risperidone (0.01 mg/kg i.p.). Furthermore, accumbal TMEM168 overexpression decreased the basal levels of extracellular GABA in the NAc and the high K+ (100 mM)-stimulated GABA elevation; however, the total contents of GABA in the NAc remained unaffected. These results suggest that the TMEM168-regulated GABAergic neuronal system in the NAc might become a novel target while studying the etiology of anxiety and sensorimotor gating deficits. | |||||
引用 | ||||||
内容記述タイプ | Other | |||||
内容記述 | PLoS ONE 12(12): e0189006. | |||||
書誌情報 |
PLos ONE 巻 12, 号 12, 発行日 2017-12-06 |
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ISSN | ||||||
収録物識別子タイプ | ISSN | |||||
収録物識別子 | 1932-6203 | |||||
DOI | ||||||
関連タイプ | isVersionOf | |||||
識別子タイプ | DOI | |||||
関連識別子 | info:doi/10.1371/journal.pone.0189006 | |||||
著者版フラグ | ||||||
出版タイプ | AM | |||||
出版タイプResource | http://purl.org/coar/version/c_ab4af688f83e57aa | |||||
出版者 | ||||||
出版者 | Public Library of Science | |||||
資源タイプ(DSpace) | ||||||
内容記述タイプ | Other | |||||
内容記述 | Article |