Premium
Regulation of AMPA receptor channels and synaptic plasticity by cofilin phosphatase Slingshot in cortical neurons
Author(s) -
Yuen Eunice Y.,
Liu Wenhua,
Kafri Tal,
Van Praag Henriette,
Yan Zhen
Publication year - 2010
Publication title -
the journal of physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.802
H-Index - 240
eISSN - 1469-7793
pISSN - 0022-3751
DOI - 10.1113/jphysiol.2009.186353
Subject(s) - cofilin , ampa receptor , neurotransmission , synaptic plasticity , microbiology and biotechnology , chemistry , excitatory postsynaptic potential , neuroscience , postsynaptic potential , actin remodeling of neurons , actin cytoskeleton , biology , cytoskeleton , glutamate receptor , inhibitory postsynaptic potential , receptor , biochemistry , cell
Cofilin, the major actin depolymerizing factor, modulates actin dynamics that contribute to spine morphology, synaptic transmission and plasticity. Much evidence implicates the cofilin inactivation kinase LIMK in synaptic function, but little is known about the cofilin activation phosphatase Slingshot in this regard. In this study, we found that suppressing endogenous Slingshot with small RNA interference or function‐blocking antibody led to a dramatic reduction of AMPA receptor‐mediated excitatory postsynaptic currents (EPSCs) in cortical neurons. Perturbation of Slingshot function also diminished the ability to express synaptic plasticity. Inactivating cofilin or disturbing actin dynamics reduced AMPAR‐EPSCs in a Slingshot‐dependent manner. Moreover, surface GluR 1 and synaptic GluR2/3 clusters were reduced by Slingshot knockdown. Our data suggest that Slingshot plays a pivotal role in AMPAR trafficking and synaptic transmission by controlling actin cytoskeleton via cofilin activation.