Subcellular organization of camkii in rat hippocampal pyramidal neurons
Open accessAbstract
Calcium/calmodulin-dependent protein kinase II (CaMKII) plays a key role in N-methyl-D-aspartate (NMDA) receptor-dependent long-term synaptic plasticity; its location is critical for signal transduction, and may provide clues that further elucidate its function. We therefore examined the subcellular localization of CaMKII in CA1 stratum radiatum of adult rat hippocampus, by using immuno-electron microscopy after chemical fixation. When tissue was fixed quickly, the concentration of CaMKIIα (assessed by pre-embedding immunogold) was significantly higher in dendritic shafts than in spine heads. However, when tissue was fixed 5 minutes after perfusion with normal saline, the density of labeling decreased in dendritic shaft while increasing in spine heads, implying rapid translocation into the spine during brief perimortem stress. Likewise, in quickly fixed tissue, CaMKII within spine heads was found at comparable concentrations in the "proximal" half (adjacent to the spine neck) and the "distal" half (containing the postsynaptic density [PSD]), whereas after delayed fixation, label density increased in the distal side of the spine head, suggesting that CaMKII within the spine head moves toward the PSD during this interval. To estimate its distribution at the synapse in vivo, we performed postembedding immunogold staining for CaMKII in quick-fixed tissue, and found that the enzyme did not concentrate primarily within the central matrix of the PSD. Instead, labeling density peaked ∼40 nm inside the postsynaptic membrane, at the cytoplasmic fringe of the PSD. Labeling within 25 nm of the postsynaptic membrane concentrated at the lateral edge of the synapse. This lateral "PSD core" pool of CaMKII may play a special role in synaptic plasticity.
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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 [140]
The Results section (‘Prolonged saline flush causes cytoplasmic redistribution of CaMKII’; page unavailable) reports CaMKII movement into spine heads and toward the postsynaptic density after a five-minute saline flush in rat hippocampal tissue. It does not report glutamate treatment of neuronal cultures. The Discussion (‘Technical issues’; page unavailable) says excessive glutamate-receptor activation is only one possible trigger of the reorganization, not an established cause in this experiment. (LLM, conf=0.88)
Experimental — accuracy not yet measuredActivation 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 [140]
The Results (‘Prolonged saline flush causes cytoplasmic redistribution of CaMKII’; page unavailable) report movement toward the PSD within five minutes of a saline flush. The Discussion (‘Technical issues’; page unavailable) says the trigger remains unclear, so the paper does not establish that CaMKII activation causes that translocation. (LLM, conf=0.86)
Experimental — accuracy not yet measured
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- Authors
- Ding, J., Kennedy, M. B., & Weinberg, R. J.
- Affiliations
- Department of Ophthalmology Duke University Medical Center Durham North Carolina 27710
- California Institute of Technology (US)
- University of North Carolina at Chapel Hill (US)
- Venue
- Journal of Comparative Neurology
- Publisher
- Wiley
- Published
- 2013-08-23
- Volume
- 521
- Issue
- 15
- Pages
- 3570-3583
- ISSN
- 0021-9967 (ISSN-L)
- 1096-9861
- PMC
- PMC4409980
- OpenAlex
- W1592516566
- Cited by
- 45
- References
- 53
- Citations by year
- 2026: 1 · 2025: 2 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 4 · 2020: 14 · 2018: 3 · 2017: 2 · 2016: 2 · 2015: 6 · 2014: 3 · 2013: 2
- FWCI
- 2.13
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Comparative Neurology (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- CaltechAUTHORS (California Institute of Technology) (submittedVersion)
- Funders
- National Institute of Neurological Disorders and Stroke (R01NS039444, P01 NS44306, R01 NS35527, R01NS035527, P01NS044306)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Protein Kinase Regulation and GTPase Signaling
- Keywords
- CaMKII, subcellular localization, hippocampal pyramidal neurons, dendritic spines, postsynaptic density, synaptic plasticity, NMDA receptor, postsynaptic membrane, CA1 stratum radiatum
- MeSH terms
- Animals, Antibodies, Cell Membrane, Cytoplasm, Data Interpretation, Statistical, Dendrites, Hippocampus, Image Processing, Computer-Assisted, Immunohistochemistry, Subcellular Fractions, Synapses, Microscopy, Immunoelectron, Tissue Embedding, Tissue Fixation, Rats, Sprague-Dawley, Pyramidal Cells, Dendritic Spines, Rats, Calcium-Calmodulin-Dependent Protein Kinase Type 2
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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