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Increased PKMζ activity impedes lateral movement of GluA2-containing AMPA receptors

Protein kinase M zeta (PKMζ), a constitutively active, atypical protein kinase C isoform, maintains a high level of expression in the brain after the induction of learning and long-term potentiation (LTP). Further, its overexpression enhances long-term memory and LTP. Thus, multiple lines of evidenc...

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Autores principales: Yu, Nam-Kyung, Uhm, Heesoo, Shim, Jaehoon, Choi, Jun-Hyeok, Bae, Sangsu, Sacktor, Todd Charlton, Hohng, Sungchul, Kaang, Bong-Kiun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: BioMed Central 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716381/
https://www.ncbi.nlm.nih.gov/pubmed/29202853
http://dx.doi.org/10.1186/s13041-017-0334-7
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author Yu, Nam-Kyung
Uhm, Heesoo
Shim, Jaehoon
Choi, Jun-Hyeok
Bae, Sangsu
Sacktor, Todd Charlton
Hohng, Sungchul
Kaang, Bong-Kiun
author_facet Yu, Nam-Kyung
Uhm, Heesoo
Shim, Jaehoon
Choi, Jun-Hyeok
Bae, Sangsu
Sacktor, Todd Charlton
Hohng, Sungchul
Kaang, Bong-Kiun
author_sort Yu, Nam-Kyung
collection PubMed
description Protein kinase M zeta (PKMζ), a constitutively active, atypical protein kinase C isoform, maintains a high level of expression in the brain after the induction of learning and long-term potentiation (LTP). Further, its overexpression enhances long-term memory and LTP. Thus, multiple lines of evidence suggest a significant role for persistently elevated PKMζ levels in long-term memory. The molecular mechanisms of how synaptic properties are regulated by the increase in PKMζ, however, are still largely unknown. The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR) mediates most of the fast glutamatergic synaptic transmission in the brain and is known to be critical for the expression of synaptic plasticity and memory. Importance of AMPAR trafficking has been implicated in PKMζ-mediated cellular processes, but the detailed mechanisms, particularly in terms of regulation of AMPAR lateral movement, are not well understood. In the current study, using a single-molecule live imaging technique, we report that the overexpression of PKMζ in hippocampal neurons immobilized GluA2-containing AMPARs, highlighting a potential novel mechanism by which PKMζ may regulate memory and synaptic plasticity.
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spelling pubmed-57163812017-12-08 Increased PKMζ activity impedes lateral movement of GluA2-containing AMPA receptors Yu, Nam-Kyung Uhm, Heesoo Shim, Jaehoon Choi, Jun-Hyeok Bae, Sangsu Sacktor, Todd Charlton Hohng, Sungchul Kaang, Bong-Kiun Mol Brain Short Report Protein kinase M zeta (PKMζ), a constitutively active, atypical protein kinase C isoform, maintains a high level of expression in the brain after the induction of learning and long-term potentiation (LTP). Further, its overexpression enhances long-term memory and LTP. Thus, multiple lines of evidence suggest a significant role for persistently elevated PKMζ levels in long-term memory. The molecular mechanisms of how synaptic properties are regulated by the increase in PKMζ, however, are still largely unknown. The α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptor (AMPAR) mediates most of the fast glutamatergic synaptic transmission in the brain and is known to be critical for the expression of synaptic plasticity and memory. Importance of AMPAR trafficking has been implicated in PKMζ-mediated cellular processes, but the detailed mechanisms, particularly in terms of regulation of AMPAR lateral movement, are not well understood. In the current study, using a single-molecule live imaging technique, we report that the overexpression of PKMζ in hippocampal neurons immobilized GluA2-containing AMPARs, highlighting a potential novel mechanism by which PKMζ may regulate memory and synaptic plasticity. BioMed Central 2017-11-29 /pmc/articles/PMC5716381/ /pubmed/29202853 http://dx.doi.org/10.1186/s13041-017-0334-7 Text en © The Author(s). 2017 Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
spellingShingle Short Report
Yu, Nam-Kyung
Uhm, Heesoo
Shim, Jaehoon
Choi, Jun-Hyeok
Bae, Sangsu
Sacktor, Todd Charlton
Hohng, Sungchul
Kaang, Bong-Kiun
Increased PKMζ activity impedes lateral movement of GluA2-containing AMPA receptors
title Increased PKMζ activity impedes lateral movement of GluA2-containing AMPA receptors
title_full Increased PKMζ activity impedes lateral movement of GluA2-containing AMPA receptors
title_fullStr Increased PKMζ activity impedes lateral movement of GluA2-containing AMPA receptors
title_full_unstemmed Increased PKMζ activity impedes lateral movement of GluA2-containing AMPA receptors
title_short Increased PKMζ activity impedes lateral movement of GluA2-containing AMPA receptors
title_sort increased pkmζ activity impedes lateral movement of glua2-containing ampa receptors
topic Short Report
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5716381/
https://www.ncbi.nlm.nih.gov/pubmed/29202853
http://dx.doi.org/10.1186/s13041-017-0334-7
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