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演題詳細

Poster

ワーキングングメモリ・実行機能
Working Memory and Executive Function

開催日 2014/9/13
時間 11:00 - 12:00
会場 Poster / Exhibition(Event Hall B)

グリア型グルタミン酸トランスポーターGLT-1を前頭前野特異的に欠損したマウスは統合失調症様の行動異常を引き起こす
Prefrontal cortex-specific deletion of glial glutamate transporter GLT-1 causes behavioral changes relevant to schizophrenia in mice

  • P3-233
  • 橋本 真理子 / Mariko Hashimoto:1 相澤 秀紀 / Hidenori Aizawa:1 相田 知海 / Tomomi Aida:1 崔 万鵬 / Wanpeng Cui:1 水上 浩明 / Hiroaki Mizukami:2 小澤 敬也 / Kinya Ozawa:2 野村 政壽 / Masatoshi Nomura:3 高柳 涼一 / Ryuichi Takayanagi:3 田中 光一 / Kohichi Tanaka:1,4,5 
  • 1:東医歯大難治疾患研分子神経科学 / Lab of Mol Neurosci, Med Res Inst, Tokyo Med Dent Univ, Tokyo, Japan 2:自治医大遺伝子治療研究部 / Div of Genet Therapeutics, Cent Mo Med, Jichi Med Univ, Tochigi, Japan 3:九州大医病態制御内科学分野 / Dept of Med Bioreg, Grad Sch Med Sci, Kyushu Univ, Fukuoka, Japan 4:科学技術振興機構 / JST, CREST, Saitama, Japan 5:東医歯大脳統合機能研セ / Cent Brain Int Res, Tokyo Med Dent Univ, Tokyo, Japan 

Schizophrenia patients carrying a common single nucleotide polymorphism in glial glutamate transporter GLT-1, which leads to reduced expression of GLT-1, are reported to show poor performance of working memory task, one of the cognitive symptoms of schizophrenia. Despite a primary role of GLT-1 in clearance of extracellular glutamate, the etiologic role of GLT-1 for cognitive dysfunctions in schizophrenia remains unclear. Since medial prefrontal cortex (mPFC) is essential region for working memory, we hypothesized that impairment of GLT-1 activity in mPFC causes behavioral changes relevant to the cognitive dysfunction in schizophrenia. To address this, mPFC-specific GLT-1 conditional knockout (cKO) was generated by injecting adeno-associated virus expressing Cre into mPFC of floxed GLT-1 mice. We observed the significant reduction of GLT-1 protein in mPFC of GLT-1 cKO four weeks after injection. Behavioral analyses revealed that mPFC-specific GLT-1 cKO mice specifically showed the impairment of spontaneous alternation in Y-maze test and pre-pulse inhibition in startle response test. These results suggested that reduction of GLT-1 activity in mPFC caused cognitive dysfunction relevant to the schizophrenia, such as deficits in working memory and sensorimotor gating.

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