Participation of Ca 2+ -Permeable AMPA Receptors in Synaptic Plasticity
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Participation of Ca2+-Permeable AMPA Receptors in Synaptic Plasticity L. P. Dolgachevaa, *, S. T. Tuleukhanovb, and V. P. Zinchenkoa, ** a
Institute of Cell Biophysics of the Russian Academy of Sciences, Pushchino, Moscow oblast, 142290 Russia b Al-Farabi Kazakh National University, Almaty, 050040 Kazakhstan *e-mail: [email protected] **e-mail: [email protected] Received April 26, 2019; revised December 17, 2019; accepted December 23, 2019
Abstract—AMPA receptors are the key molecules of excitatory and inhibitory synapses and are involved in synaptic plasticity. Cognitive functions of the brain such as signal perception, processing and analysis of information, memory, storage and exchange of information are reduced when the processes controlling the assembly of AMPA receptors, membrane trafficking and synapse-specific expression are impaired. The content of the receptors in synapses is regulated by exocytosis, endocytosis, and receptor recycling. Auxiliary subunits and partners modulate the function of AMPA receptors. Ca2+-permeable AMPA receptors (CP-AMPAR) not containing the GluA2 subunit are involved in multiple forms of the synaptic plasticity, including longterm potentiation and depression, and play an important role in maintaining the correct balance between excitation and inhibition in the brain. The activation of CP-AMPAR in neurons provides a fast postsynaptic Ca2+ entry, which triggers the processes modifying synaptic functions through the interaction with other Ca2+-transporting systems. The purpose of this review is to draw the attention of researchers to recent advances in the participation of CP-AMPA receptors in synaptic plasticity. Keywords: Ca2+-permeable AMPA receptors, glutamate receptors, interneurons, synapse, synaptic plasticity, long-term potentiation, auxiliary subunits, neurodegeneration, polyamines, polyamine block DOI: 10.1134/S1990747820030046
INTRODUCTION AMPA-type glutamate receptors are classically considered to be the receptor channels depolarizing the membrane due to Na+ permeability, which allows excitatory signals to pass through neuronal synapses and leads to the activation of voltage-gated calcium channels and the removal of the Mg2+ block of NMDA receptors. However, separate subpopulations of AMPA receptors lacking the GluA2 subunit, have calcium permeability, which does not depend on the membrane potential [1] so that the process of neurotransmitter release can be triggered without depolarization and involvement of voltage-dependent calcium and NMDA channels. The Ca2+ permeability of these receptors is of crucial importance for some forms of synaptic plasticity [1, 2] and cell death caused by neuAbbreviations: AMPARs, α-amino-3-hydroxy-5-methyl-4-isoxazole propionic acid receptors; TARP, transmembrane AMPA receptor regulatory proteins; CNIH, Cornichon homolog; GSG1L, transmembrane auxiliary protein (Germline-specific gene 1-like); CKAMP, Cystine-knot AMPA receptor-modulating proteins; AKAP, A-kinase anchoring protein; PSD-95, postsynaptic density protein; LTP, long-term poten
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