ArticleBrain research2011
Quantitative estimates of the cytoplasmic, PSD, and NMDAR-bound pools of CaMKII in dendritic spines.
Article in Brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
25 citing papers in PubMed, 47 citations in OpenAlex.
- 40 Hz light preserves synaptic plasticity and mitochondrial function in Alzheimer's disease model.Scientific reports · 2024Article
- Synaptic memory and CaMKII.Physiological reviews · 2023Review
- A stochastic model of hippocampal synaptic plasticity with geometrical readout of enzyme dynamics.eLife · 2023Article
- CaMKIIα as a Promising Drug Target for Ischemic Grey Matter.Brain sciences · 2022Review
- A Modeling and Analysis Study Reveals That CaMKII in Synaptic Plasticity Is a Dominant Affecter in CaM Systems in a T286 Phosphorylation-Dependent Manner.Molecules (Basel, Switzerland) · 2022Article
- High levels of 27-hydroxycholesterol results in synaptic plasticity alterations in the hippocampus.Scientific reports · 2021Article
- Neuroprotective Effects of Salidroside in a Mouse Model of Alzheimer's Disease.Cellular and molecular neurobiology · 2020Article
- CaMKII versus DAPK1 Binding to GluN2B in Ischemic Neuronal Cell Death after Resuscitation from Cardiac Arrest.Cell reports · 2020Article
- Arc Oligomerization Is Regulated by CaMKII Phosphorylation of the GAG Domain: An Essential Mechanism for Plasticity and Memory Formation.Molecular cell · 2019Article
- Reciprocal Activation within a Kinase-Effector Complex Underlying Persistence of Structural LTP.Neuron · 2019Article
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- Biochemical principles underlying the stable maintenance of LTP by the CaMKII/NMDAR complex.Brain research · 2015Article
- Signaling to the microtubule cytoskeleton: an unconventional role for CaMKII.Developmental neurobiology · 2015Review
- Multiple spatial and kinetic subpopulations of CaMKII in spines and dendrites as resolved by single-molecule tracking PALM.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
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- Review
- Alternative splicing in the variable domain of CaMKIIβ affects the level of F-actin association in developing neurons.International journal of clinical and experimental pathology · 2014Article
- The CaMKII/NMDAR complex as a molecular memory.Molecular brain · 2013Review
- CaMKII regulation in information processing and storage.Trends in neurosciences · 2012Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
CaMKII plays a critical role in long-term potentiation (LTP). The kinase is a major component of the postsynaptic density (PSD); however, it is also contained in the spine cytoplasm. CaMKII can now be monitored optically in living neurons, and it is therefore important to understand the contribution of the PSD and cytoplasmic pools to optical signals. Here, we estimate the size of these pools under basal conditions. From EM immunolabeling data, we calculate that the PSD/cytoplasmic ratio is ~5%. A second independent estimate is derived from measurements indicating that the average mushroom spine PSD contains 90 to 240 holoenzymes. A cytoplasmic concentration of 16 μM (~2590 holoenzymes) in the spine can be estimated from the total measured CaMKII content of hippocampal tissue, the relative volume of different compartments, and the spine-dendrite ratio of CaMKII (2:1). These numbers yield a second estimate (6%) of the PSD/spine ratio in good agreement with the first. The CaMKII bound to the NMDAR is important because preventing the formation of this complex blocks LTP induction. We estimate that the percentage of spine CaMKII held active by binding to the NMDAR is ~0.2%. Implications of the high spine concentration of CaMKII (> 100 μM alpha subunits) and the small fraction within the PSD are discussed. Of particular note, the finding that the CaMKII signal in spines shows only transient activation (open state) after LTP induction is subject to the qualification that it does not reflect the small but important pool bound to the NMDAR.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.