Format

Send to

Choose Destination
Mol Brain. 2017 Nov 29;10(1):56. doi: 10.1186/s13041-017-0334-7.

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

Yu NK1, Uhm H2,3,4,5, Shim J1, Choi JH1, Bae S6, Sacktor TC7,8,9, Hohng S10,11,12,13, Kaang BK14,15.

Author information

1
Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul, South Korea.
2
Department of Physics and Astronomy, Seoul National University, Seoul, South Korea.
3
National Center for Creative Research Initiatives, Seoul National University, Seoul, South Korea.
4
Institute of Applied Physics, Seoul National University, Seoul, South Korea.
5
Department of Biophysics and Chemical Biology, Seoul National University, Seoul, South Korea.
6
Institute of Nano Science and Technology, Hanyang University, Seoul, South Korea.
7
Department of Physiology & Pharmacology, SUNY Downstate Medical Center, 450 Clarkson Ave, Brooklyn, NY, 11203, USA.
8
Department of Anesthesiology, SUNY Downstate Medical Center, 450 Clarkson Ave, Brooklyn, NY, 11203, USA.
9
Department of Neurology, SUNY Downstate Medical Center, 450 Clarkson Ave, Brooklyn, NY, 11203, USA.
10
Department of Physics and Astronomy, Seoul National University, Seoul, South Korea. shhong@snu.ac.kr.
11
National Center for Creative Research Initiatives, Seoul National University, Seoul, South Korea. shhong@snu.ac.kr.
12
Institute of Applied Physics, Seoul National University, Seoul, South Korea. shhong@snu.ac.kr.
13
Department of Biophysics and Chemical Biology, Seoul National University, Seoul, South Korea. shhong@snu.ac.kr.
14
Department of Biological Sciences, College of Natural Sciences, Seoul National University, Seoul, South Korea. kaang@snu.ac.kr.
15
Center for Neuron and Disease, Frontier Institute of Life Science and of Science and Technology, Xi'an Jiaotong University, Xi'an, China. kaang@snu.ac.kr.

Abstract

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.

KEYWORDS:

AMPAR; GluA2; LTP; Lateral diffusion; PKM-zeta; PKMζ; Quantum dots; Single molecule imaging

PMID:
29202853
PMCID:
PMC5716381
DOI:
10.1186/s13041-017-0334-7
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for BioMed Central Icon for PubMed Central
Loading ...
Support Center