Learning, AMPA receptor mobility and synaptic plasticity depend on n-cofilin-mediated actin dynamics

Marco B Rust, Christine B Gurniak, Marianne Renner, Hugo Vara, Laura Morando, Andreas Görlich, Marco Sassoè-Pognetto, Mumna Al Banchaabouchi, Maurizio Giustetto, Antoine Triller, Daniel Choquet, Walter Witke
EMBO J. 2010-04-20; 29(11): 1889-1902
DOI: 10.1038/emboj.2010.72

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Neuronal plasticity is an important process for learning, memory and complex
behaviour. Rapid remodelling of the actin cytoskeleton in the postsynaptic
compartment is thought to have an important function for synaptic plasticity.
However, the actin-binding proteins involved and the molecular mechanisms that in
vivo link actin dynamics to postsynaptic physiology are not well understood.
Here, we show that the actin filament depolymerizing protein n-cofilin is
controlling dendritic spine morphology and postsynaptic parameters such as late
long-term potentiation and long-term depression. Loss of n-cofilin-mediated
synaptic actin dynamics in the forebrain specifically leads to impairment of all
types of associative learning, whereas exploratory learning is not affected. We
provide evidence for a novel function of n-cofilin function in synaptic
plasticity and in the control of extrasynaptic excitatory AMPA receptors
diffusion. These results suggest a critical function of actin dynamics in
associative learning and postsynaptic receptor availability.


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