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Molecular motor KIF17 is fundamental for memory and learning via differential support of synaptic NR2A/2B levels

Xiling Yin1, Yosuke Takei, Mizuho A Kido

  • 1Department of Cell Biology and Anatomy, Graduate School of Medicine, The University of Tokyo, 7-3-1 Hongo, Bunkyo-ku, Tokyo 113-0033, Japan.

Neuron
|April 28, 2011
PubMed

Insights

Kinesin superfamily motor protein 17 (KIF17) transports NMDA receptor subunit 2B (NR2B). Loss of KIF17 impairs NR2B and NR2A levels, disrupting synaptic function and hippocampus-dependent memory.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Kinesin superfamily motor protein 17 (KIF17) is implicated in the transport of N-methyl-D-aspartate (NMDA) receptor subunit 2B (NR2B).
  • The precise role of KIF17 in regulating NMDA receptor subunit levels and synaptic plasticity remains incompletely understood.

Purpose of the Study:

  • To investigate the function of KIF17 in the transport and regulation of NR2B and NR2A subunits.
  • To elucidate the impact of KIF17 disruption on synaptic function, neuronal plasticity, and memory.

Main Methods:

  • Utilized knockout mouse models (kif17(-/-)) to study KIF17 function.
  • Assessed NR2B and NR2A levels, synaptic currents, and long-term potentiation/depression in hippocampal neurons.
  • Evaluated CREB responses and hippocampus-dependent memory performance in knockout mice.

Main Results:

  • Disruption of KIF17 inhibited NR2B transport and decreased NR2B transcription, leading to reduced synaptic NR2B.
  • KIF17 deficiency also decreased NR2A levels via accelerated ubiquitin-proteasome degradation.
  • NMDA receptor-mediated currents, synaptic plasticity, CREB activation, and memory were impaired in kif17(-/-) mice.

Conclusions:

  • KIF17 plays a critical role in maintaining synaptic levels of both NR2A and NR2B subunits.
  • KIF17-dependent mechanisms regulate synaptic plasticity and are essential for hippocampus-dependent memory formation and retrieval.

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