Involvement of Ca2+ channel synprint site in synaptic vesicle endocytosis

Hiroyasu Watanabe, Takayuki Yamashita, Naoto Saitoh, Shigeki Kiyonaka, Akihiro Iwamatsu, Kevin P. Campbell, Yasuo Mori, Tomoyuki Takahashi

研究成果: Article査読

23 被引用数 (Scopus)

抄録

The synaptic protein interaction (synprint) site of the voltage-gated Ca2+channel (VGCC) α1 subunit can interact with proteins involved in exocytosis, and it is therefore thought to be essential for exocytosis of synaptic vesicles. Here we report that the synprint site can also directly bind the μ subunit of AP-2, an adaptor protein for clathrin-mediated endocytosis, in competition with the synaptotagmin 1 (Syt 1) C2B domain. In brain lysates, the AP-2-synprint interaction occurred over a wide range of Ca2+ concentrations but was inhibited at high Ca2+ concentrations, in which Syt 1 interacted with synprint site. At the calyx of Held synapse in rat brainstem slices, direct presynaptic loading of the synprint fragment peptide blocked endocytic, but not exocytic, membrane capacitance changes. We propose that the VGCC synprint site is involved in synaptic vesicle endocytosis, rather than exocytosis, in the nerve terminal, via Ca 2+-dependent interactions with AP-2 and Syt.

本文言語English
ページ(範囲)655-660
ページ数6
ジャーナルJournal of Neuroscience
30
2
DOI
出版ステータスPublished - 13-01-2010
外部発表はい

All Science Journal Classification (ASJC) codes

  • 神経科学(全般)

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