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      Balance and stability of synaptic structures during synaptic plasticity.

      Neuron
      Animals, Animals, Newborn, CA1 Region, Hippocampal, cytology, Carrier Proteins, metabolism, Dendritic Spines, ultrastructure, Glutamic Acid, pharmacology, Green Fluorescent Proteins, genetics, Intracellular Signaling Peptides and Proteins, Membrane Proteins, Neuronal Plasticity, drug effects, physiology, Neurons, Organ Culture Techniques, Plant Lectins, Post-Synaptic Density, Rats, Rats, Wistar, Synapses, Time Factors, Transduction, Genetic

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          Abstract

          Subsynaptic structures such as bouton, active zone, postsynaptic density (PSD) and dendritic spine, are highly correlated in their dimensions and also correlate with synapse strength. Why this is so and how such correlations are maintained during synaptic plasticity remains poorly understood. We induced spine enlargement by two-photon glutamate uncaging and examined the relationship between spine, PSD, and bouton size by two-photon time-lapse imaging and electron microscopy. In enlarged spines the PSD-associated protein Homer1c increased rapidly, whereas the PSD protein PSD-95 increased with a delay and only in cases of persistent spine enlargement. In the case of nonpersistent spine enlargement, the PSD proteins remained unchanged or returned to their original level. The ultrastructure at persistently enlarged spines displayed matching dimensions of spine, PSD, and bouton, indicating their correlated enlargement. This supports a model in which balancing of synaptic structures is a hallmark for the stabilization of structural modifications during synaptic plasticity. Copyright © 2014 Elsevier Inc. All rights reserved.

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