A kinesin 1-protrudin complex mediates AMPA receptor synaptic removal during long-term depression
Standard
A kinesin 1-protrudin complex mediates AMPA receptor synaptic removal during long-term depression. / Brachet, Anna; Lario, Argentina; Fernández-Rodrigo, Alba; Heisler, Frank F; Gutiérrez, Yolanda; Lobo, Clara; Kneussel, Matthias; Esteban, José A.
In: CELL REP, Vol. 36, No. 5, 109499, 03.08.2021.Research output: SCORING: Contribution to journal › SCORING: Journal article › Research › peer-review
Harvard
APA
Vancouver
Bibtex
}
RIS
TY - JOUR
T1 - A kinesin 1-protrudin complex mediates AMPA receptor synaptic removal during long-term depression
AU - Brachet, Anna
AU - Lario, Argentina
AU - Fernández-Rodrigo, Alba
AU - Heisler, Frank F
AU - Gutiérrez, Yolanda
AU - Lobo, Clara
AU - Kneussel, Matthias
AU - Esteban, José A
N1 - Copyright © 2021 The Authors. Published by Elsevier Inc. All rights reserved.
PY - 2021/8/3
Y1 - 2021/8/3
N2 - The synaptic removal of AMPA-type glutamate receptors (AMPARs) is a core mechanism for hippocampal long-term depression (LTD). In this study, we address the role of microtubule-dependent transport of AMPARs as a driver for vesicular trafficking and sorting during LTD. Here, we show that the kinesin-1 motor KIF5A/C is strictly required for LTD expression in CA3-to-CA1 hippocampal synapses. Specifically, we find that KIF5 is required for an efficient internalization of AMPARs after NMDA receptor activation. We show that the KIF5/AMPAR complex is assembled in an activity-dependent manner and associates with microsomal membranes upon LTD induction. This interaction is facilitated by the vesicular adaptor protrudin, which is also required for LTD expression. We propose that protrudin links KIF5-dependent transport to endosomal sorting, preventing AMPAR recycling to synapses after LTD induction. Therefore, this work identifies an activity-dependent molecular motor and the vesicular adaptor protein that executes AMPAR synaptic removal during LTD.
AB - The synaptic removal of AMPA-type glutamate receptors (AMPARs) is a core mechanism for hippocampal long-term depression (LTD). In this study, we address the role of microtubule-dependent transport of AMPARs as a driver for vesicular trafficking and sorting during LTD. Here, we show that the kinesin-1 motor KIF5A/C is strictly required for LTD expression in CA3-to-CA1 hippocampal synapses. Specifically, we find that KIF5 is required for an efficient internalization of AMPARs after NMDA receptor activation. We show that the KIF5/AMPAR complex is assembled in an activity-dependent manner and associates with microsomal membranes upon LTD induction. This interaction is facilitated by the vesicular adaptor protrudin, which is also required for LTD expression. We propose that protrudin links KIF5-dependent transport to endosomal sorting, preventing AMPAR recycling to synapses after LTD induction. Therefore, this work identifies an activity-dependent molecular motor and the vesicular adaptor protein that executes AMPAR synaptic removal during LTD.
U2 - 10.1016/j.celrep.2021.109499
DO - 10.1016/j.celrep.2021.109499
M3 - SCORING: Journal article
C2 - 34348158
VL - 36
JO - CELL REP
JF - CELL REP
SN - 2211-1247
IS - 5
M1 - 109499
ER -