AMPAR trafficking in synapse maturation and plasticity
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Cellular and Molecular Life Sciences
Review
AMPAR trafficking in synapse maturation and plasticity Silvia Bassani · Alessandra Folci · Jonathan Zapata · Maria Passafaro
Received: 25 October 2012 / Revised: 15 February 2013 / Accepted: 18 February 2013 © Springer Basel 2013
Abstract Glutamate ionotropic alpha-amino-3-hydroxy5-methyl-4-isoxazole propionic acid (AMPA) receptors (AMPARs) mediate most fast excitatory synaptic transmission in the central nervous system. The content and composition of AMPARs in postsynaptic membranes (which determine synaptic strength) are dependent on the regulated trafficking of AMPAR subunits in and out of the membranes. AMPAR trafficking is a key mechanism that drives nascent synapse development, and is the main determinant of both Hebbian and homeostatic plasticity in mature synapses. Hebbian plasticity seems to be the biological substrate of at least some forms of learning and memory; while homeostatic plasticity (also known as synaptic scaling) keeps neuronal circuits stable by maintaining changes within a physiological range. In this review, we examine recent findings that provide further understanding of the role of AMPAR trafficking in synapse maturation, Hebbian plasticity, and homeostatic plasticity. Keywords AMPAR trafficking · Synaptic plasticity · Synapse maturation
S. Bassani, A. Folci, and J. Zapata contributed equally to this work. S. Bassani · A. Folci · J. Zapata · M. Passafaro (*) CNR Institute of Neuroscience, Department of Medical Pharmacology, University of Milan, Milan, Italy e-mail: [email protected] M. Passafaro Dulbecco Telethon Institute, Rome, Italy
Introduction Glutamatergic synapses mediate excitatory transmission in the central nervous system. Alpha-amino-3-hydroxy5-methyl-4-isoxazole propionic acid (AMPA) receptors (AMPARs) and N-methyl-d-aspartate (NMDA) receptors (NMDARs) are the two principal types of ionotropic glutamate receptors in glutamatergic synapses, and changes in the trafficking, subunit composition, and signaling of these receptors are fundamental processes underlying synapse strength. AMPARs are tetrameric cation channels that mediate fast excitatory synaptic transmission in the mammalian central nervous system [1]. NMDARs are also tetrameric cation channels; their activation requires glutamate (ligand-gating) and also membrane depolarization (voltagedependence), which removes the Mg2+ normally blocking the channel. Activated NMDARs allow Ca2+ to enter the neuron; the magnitude of the Ca2+ signal in the postsynaptic neuron largely determines whether long-term potentiation (LTP) or long-term depression (LTD) of AMPAR currents occurs [2]. During synaptogenesis, the subunit composition and relative abundance of AMPA and NMDA receptors are adjusted as crucial steps in the establishment of a functionally mature synapse. In younger neurons, the synapses are characterized by low AMPAR/NMDAR ratio. Maturation is marked by incorporation of NMDARs containing the GluNA2 subunit into the synapse and an increase in the AMPA/NMDA current r
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