KIF17‐mediated transport of NMDA receptors and schizophrenia

  • Takei Yosuke
    Laboratory of Anatomy and Neuroscience, Faculty of Medicine, University of Tsukuba
  • Tome Saki
    Laboratory of Anatomy and Neuroscience, Faculty of Medicine, University of Tsukuba
  • Sasaki Tetsuya
    Laboratory of Anatomy and Neuroscience, Faculty of Medicine, University of Tsukuba

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Other Title
  • NMDA型グルタミン酸受容体の細胞内輸送と統合失調症
  • NMDAガタ グルタミンサン ジュヨウタイ ノ サイボウ ナイ ユソウ ト トウゴウ シッチョウショウ

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Description

Neurons make a neural network and communicate each other via their synapses. Synaptic accumulation of neurotransmitter receptors is necessary for efficient neurotransmission. A member of kinesin superfamily proteins (KIFs) KIF17 transports NMDA receptor subunit 2B in dendrites. KIF17 is essential for neuronal plasticity such as long‐term potentiation (LTP) and long‐term depression (LTD) in hippocampus. Lack of KIF17 resulted in memory disturbances in mice. Transport of NMDA receptors is regulated by phosphorylation and CREB‐mediated upregulation of motor and cargoes in an activity‐dependent manner. The transport of NMDA receptors was also supported by a non‐motor microtubule‐associated protein MAP1A. These multiple ways of regulation of NMDA‐receptor transport support neuronal plasticity and brain function such as learning and memory. Recently, lines of evidence from genetic and post‐mortem examination approaches indicate that compromised NMDA receptor function in schizophrenia might be linked to alteration in KIF17‐mediated transport of NMDA receptor. Further translational research is needed to elucidate the contribution of KIF17 to the pathogenesis and pathophysiology of schizophrenia.

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