ID | 60769 |
フルテキストURL | |
著者 |
Sumi, Tomonari
Research Institute for Interdisciplinary Science, Okayama University
ORCID
Kaken ID
publons
researchmap
Harada, Kouji
Department of Computer Science and Engineering, Toyohashi University of Technology
|
抄録 | N-methyl-D-aspartate (NMDA) receptor-dependent long-term potentiation (LTP) and long-term depression (LTD) of signal transmission form neural circuits and thus are thought to underlie learning and memory. These mechanisms are mediated by AMPA receptor (AMPAR) trafficking in postsynaptic neurons. However, the regulatory mechanism of bidirectional plasticity at excitatory synapses remains unclear. We present a network model of AMPAR trafficking for adult hippocampal pyramidal neurons, which reproduces both LTP and LTD. We show that the induction of both LTP and LTD is regulated by the competition between exocytosis and endocytosis of AMPARs, which are mediated by the calcium-sensors synaptotagmin 1/7 (Syt1/7) and protein interacting with C-kinase 1 (PICK1), respectively. Our result indicates that recycling endosomes containing AMPAR are always ready for Syt1/7-dependent exocytosis of AMPAR at peri-synaptic/synaptic membranes. This is because molecular motor myosin V-b constitutively transports the recycling endosome toward the membrane in a Ca2+-independent manner.
|
キーワード | Biophysical models
Long-term depression
Long-term potentiation
|
発行日 | 2020-09-07
|
出版物タイトル |
Scientific Reports
|
巻 | 10巻
|
号 | 1号
|
出版者 | Nature
|
開始ページ | 14711
|
ISSN | 2045-2322
|
資料タイプ |
学術雑誌論文
|
言語 |
英語
|
OAI-PMH Set |
岡山大学
|
著作権者 | © The Author(s) 2020
|
論文のバージョン | publisher
|
PubMed ID | |
DOI | |
Web of Science KeyUT | |
関連URL | isVersionOf https://doi.org/10.1038/s41598-020-71528-3
|
ライセンス | http://creat iveco mmons .org/licenses/by/4.0/
|
助成機関名 |
日本学術振興会
|
助成番号 | JP16K05657
JP18KK0151
JP16K00389
|