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Synaptic Plasticity

開催日 2014/9/12
時間 14:00 - 15:00
会場 Poster / Exhibition(Event Hall B)

Semaphorin3A mediates learning-induced synaptic delivery of AMPAR to hippocampal CA3-CA1 synapses

  • P2-044
  • 高橋-実木 葵 / Aoi Takahashi Jitsuki:1 山下 直也 / Naoya Yamashita:1,3 実木 亨 / Susumu Jitsuki:2 五嶋 良郎 / Yoshio Goshima:1 高橋 琢哉 / Takuya Takahashi:2 
  • 1:横浜市立大学 / Dept. of Mol. Pharmacol. & Neurobiol, Grad. Sch. of Med., Yokohama City Univ., 2:横浜市立大学大学院医学研究科生理学 / Dept. Physiol., Yokohama city Univ. Grad. Sch. Med. Yokohama City Univ., 3:Department of Biology, Johns Hopkins University. USA / Department of Biology, Johns Hopkins University, USA 

Synaptic plasticity is important for the formation and stability of neuronal circuits and provides substrates for learning and memory. Several lines of evidence suggest that axon guidance molecules regulate synaptic connectivity and maintenance. We previously found that Semaphorin3A (Sema3A), a repulsive axon guidance molecule, regulates dendritic spine morphology. However, its role on synaptic plasticity is still unknown. Here, we show evidence that Sema3A signaling induces AMPA receptor (AMPAR) trafficking to regulate hippocampal learning. Over-expression of PlexinA (PlexA)-CA, which constitutively activates semaphorin signaling, increased AMPAR-mediates currents at hippocampal slices. In contrast, over-expression of dominant negative form of PlexA decreased AMPAR-mediates currents, suggesting that semaphorin signaling enhances AMPAR trafficking at hippocampal synapses. Next we focused on the learning-dependent AMPAR trafficking. We found that knock-down of PlexA4 exhibited impairment of learning-induced AMPAR trafficking, which consequently impairs learning performance. This phenotype is also seen by knock-down of Neulophilin-1 (NRP1). Since Sema3A preferentially binds to NRP1/PlexA4 complex, these results suggest that hippocampal learning activates Sema3A signaling, which induces synaptic delivery of AMPAR.

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