scholarly journals Targeted In Vivo Mutations of the AMPA Receptor Subunit GluR2 and Its Interacting Protein PICK1 Eliminate Cerebellar Long-Term Depression

Neuron ◽  
2006 ◽  
Vol 49 (6) ◽  
pp. 845-860 ◽  
Author(s):  
Jordan P. Steinberg ◽  
Kogo Takamiya ◽  
Ying Shen ◽  
Jun Xia ◽  
Maria E. Rubio ◽  
...  
eLife ◽  
2020 ◽  
Vol 9 ◽  
Author(s):  
Javier Díaz-Alonso ◽  
Wade Morishita ◽  
Salvatore Incontro ◽  
Jeffrey Simms ◽  
Julia Holtzman ◽  
...  

We tested the proposal that the C-terminal domain (CTD) of the AMPAR subunit GluA1 is required for LTP. We found that a knock-in mouse lacking the CTD of GluA1 expresses normal LTP and spatial memory, assayed by the Morris water maze. Our results support a model in which LTP generates synaptic slots, which capture passively diffusing AMPARs.


2003 ◽  
Vol 553 (3) ◽  
pp. 843-856 ◽  
Author(s):  
Vidar Jensen ◽  
Katharina M. M. Kaiser ◽  
Thilo Borchardt ◽  
Giselind Adelmann ◽  
Andrei Rozov ◽  
...  

2020 ◽  
Vol 117 (9) ◽  
pp. 4948-4958 ◽  
Author(s):  
Adeline J. H. Yong ◽  
Han L. Tan ◽  
Qianwen Zhu ◽  
Alexei M. Bygrave ◽  
Richard C. Johnson ◽  
...  

Hebbian plasticity, comprised of long-term potentiation (LTP) and depression (LTD), allows neurons to encode and respond to specific stimuli; while homeostatic synaptic scaling is a counterbalancing mechanism that enables the maintenance of stable neural circuits. Both types of synaptic plasticity involve the control of postsynaptic α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR) abundance, which is modulated by AMPAR phosphorylation. To address the necessity of GluA2 phospho-Y876 in synaptic plasticity, we generated phospho-deficient GluA2 Y876F knock-in mice. We show that, while GluA2 phospho-Y876 is not necessary for Hebbian plasticity, it is essential for both in vivo and in vitro homeostatic upscaling. Bidirectional changes in GluA2 phospho-Y876 were observed during homeostatic scaling, with a decrease during downscaling and an increase during upscaling. GluA2 phospho-Y876 is necessary for synaptic accumulation of glutamate receptor interacting protein 1 (GRIP1), a crucial scaffold protein that delivers AMPARs to synapses, during upscaling. Furthermore, increased phosphorylation at GluA2 Y876 increases GluA2 binding to GRIP1. These results demonstrate that AMPAR trafficking during homeostatic upscaling can be gated by a single phosphorylation site on the GluA2 subunit.


Neuroscience ◽  
2014 ◽  
Vol 257 ◽  
pp. 49-64 ◽  
Author(s):  
S. Katsouli ◽  
A. Stamatakis ◽  
P. Giompres ◽  
E.D. Kouvelas ◽  
F. Stylianopoulou ◽  
...  

2009 ◽  
Vol 16 (6) ◽  
pp. 379-386 ◽  
Author(s):  
D. J. Sanderson ◽  
M. A. Good ◽  
K. Skelton ◽  
R. Sprengel ◽  
P. H. Seeburg ◽  
...  

2020 ◽  
Author(s):  
Javier Díaz-Alonso ◽  
Wade Morishita ◽  
Salvatore Incontro ◽  
Jeffrey Simms ◽  
Julia Holtzman ◽  
...  

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