Glutamate-induced transient modification of the postsynaptic density

Dosemeci, Ayse; Tao-Cheng, Jung-Hwa; Vinade, Lucia; Winters, Christine A.; Pozzo-Miller, Lucas; Reese, Thomas S.

doi:10.1073/pnas.181336998

Cited by 184Neuroscience and Neuropharmacology ResearchProtein Kinase Regulation and GTPase SignalingMemory and Neural Mechanisms

Glutamate-induced transient modification of the postsynaptic density

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Dosemeci, Ayse, Tao-Cheng, Jung-Hwa, Vinade, Lucia, Winters, Christine A., Pozzo-Miller, Lucas, Reese, Thomas S.·2001·Proceedings of the National Academy of Sciences

DOI 10.1073/pnas.181336998PMC PMC56977

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Abstract

Depolarization of rat hippocampal neurons with a high concentration of external potassium induces a thickening of postsynaptic densities (PSDs) within 1.5-3 min. After high-potassium treatment, PSDs thicken 2.1-fold in cultured neurons and 1.4-fold in hippocampal slices compared with their respective controls. Thin-section immunoelectron microscopy of hippocampal cultures indicates that at least part of the observed thickening of PSDs can be accounted for by an accumulation of Ca(2+)/calmodulin-dependent protein kinase II (CaMKII) on their cytoplasmic faces. Indeed, PSD-associated gold label for CaMKII increases 5-fold after depolarization with potassium. The effects of high-potassium treatment on the composition and structure of the PSDs are mimicked by direct application of glutamate. In cultures, glutamate-induced thickening of PSDs and the accumulation of CaMKII on PSDs are reversed within 5 min of removal of glutamate and Ca(2+) from the extracellular medium. These results suggest that PSDs are dynamic structures whose thickness and composition are subject to rapid and transient changes during synaptic activity.

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Activation of CaMKII results in the rapid translocation of CaMKII to the PSD.
“activation of CaMKII results in the rapid translocation of CaMKII to the PSD (137, 140, 169, 216–220).”
From Synaptic memory and CaMKII (2023) · cites this paper as [137]
The introduction says PSDs thicken during synaptic activity partly because of CaMKII translocation, and the discussion reports that glutamate induces reversible CaMKII association with PSDs. The paper supports rapid translocation after stimulation, but does not establish that activation of CaMKII itself causes it. (LLM, conf=0.83)
Experimental — accuracy not yet measured
Glutamate treatment of neuronal cultures causes CaMKII clustering at excitatory synapses.
“Glutamate treatment of neuronal cultures causes CaMKII clustering at excitatory synapses (136–140).”
From Synaptic memory and CaMKII (2023) · cites this paper as [137]

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Authors: Dosemeci, A., Tao-Cheng, J.-H., Vinade, L., Winters, C. A., Pozzo-Miller, L., & Reese, T. S.
Affiliations: Marine Biological Laboratories, Woods Hole, MA 02543; Laboratory of Neurobiology, Electron Microscopy Facility, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892; and Department of Neurobiology, University of Alabama, Birmingham, AL 35294
National Institutes of Health (US)
ORCID: Tao-Cheng, Jung-Hwa
Reese, Thomas S.
Venue: Proceedings of the National Academy of Sciences
Publisher: National Academy of Sciences
Published: 2001-08-21
Volume: 98
Issue: 18
Pages: 10428-10432
ISSN: 0027-8424 (ISSN-L)
1091-6490
DOI: 10.1073/pnas.181336998
PMC: PMC56977
OpenAlex: W2131475149
Cited by: 184
References: 24
Citations by year: 2026: 2 · 2025: 4 · 2024: 4 · 2023: 7 · 2022: 6 · 2021: 3 · 2020: 18 · 2019: 4 · 2018: 8 · 2017: 6 · 2016: 13 · 2015: 7 · 2014: 6 · 2013: 5 · 2012: 5
FWCI: 3.33
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Locations: Proceedings of the National Academy of Sciences (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Science Foundation (9817317)
National Institutes of Health
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
Keywords: postsynaptic density, glutamate, CaMKII, hippocampal neurons, depolarization, high potassium, synaptic plasticity, calcium/calmodulin-dependent protein kinase, calcium signaling
MeSH terms: Animals, Cells, Cultured, Hippocampus, Nerve Tissue Proteins, Neurons, Potassium, Microscopy, Immunoelectron, Calcium-Calmodulin-Dependent Protein Kinases, Glutamic Acid, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2

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Glutamate-induced transient modification of the postsynaptic density

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