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Abstract
Long-term potentiation (LTP) is accompanied by dendritic spine growth and changes
in the composition of the postsynaptic density (PSD). We find that activity-dependent
growth of apical spines of CA1 pyramidal neurons is accompanied by destabilization
of the PSD that results in transient loss and rapid replacement of PSD-95 and SHANK2.
Signaling through PSD-95 is required for activity-dependent spine growth and trafficking
of SHANK2. N-terminal PDZ and C-terminal guanylate kinase domains of PSD-95 are required
for both processes, indicating that PSD-95 coordinates multiple signals to regulate
morphological plasticity. Activity-dependent trafficking of PSD-95 is triggered by
phosphorylation at serine 73, a conserved calcium/calmodulin-dependent protein kinase
II (CaMKII) consensus phosphorylation site, which negatively regulates spine growth
and potentiation of synaptic currents. We propose that PSD-95 and CaMKII act at multiple
steps during plasticity induction to initially trigger and later terminate spine growth
by trafficking growth-promoting PSD proteins out of the active spine.