ArticleFrontiers in molecular neuroscience2012
Ca(2+) sensor proteins in dendritic spines: a race for Ca(2+).
Article in Frontiers in molecular neuroscience, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 30 citations in OpenAlex.
- Myosin Va-dependent Transport of NMDA Receptors in Hippocampal Neurons.Neuroscience bulletin · 2024Article
- Caldendrin and myosin V regulate synaptic spine apparatus localization via ER stabilization in dendritic spines.The EMBO journal · 2022Article
- Stationary CaBiophysical journal · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Geometric Control of Frequency Modulation of cAMP Oscillations due to Calcium in Dendritic Spines.Biophysical journal · 2019Article
- Probing Single SynapsesFrontiers in synaptic neuroscience · 2019Article
- Caldendrin and Calneurons-EF-Hand CaM-Like Calcium Sensors With Unique Features and Specialized Neuronal Functions.Frontiers in molecular neuroscience · 2019Review
- Extension of Rapid Buffering Approximation to CaBiophysical journal · 2018Article
- Article
- Padé Approximation of a Stationary Single-Channel CaBiophysical journal · 2016Article
- Proteomics of the Synapse--A Quantitative Approach to Neuronal Plasticity.Molecular & cellular proteomics : MCP · 2016Review
- Sense and specificity in neuronal calcium signalling.Biochimica et biophysica acta · 2015Review
- Action potential processing in a detailed Purkinje cell model reveals a critical role for axonal compartmentalization.Frontiers in cellular neuroscience · 2015Article
- Article
- Input transformation by dendritic spines of pyramidal neurons.Frontiers in neuroanatomy · 2014Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Dendritic spines are believed to be micro-compartments of Ca(2+) regulation. In a recent study, it was suggested that the ubiquitous and evolutionarily conserved Ca(2+) sensor, calmodulin (CaM), is the first to intercept Ca(2+) entering the spine and might be responsible for the fast decay of Ca(2+) transients in spines. Neuronal calcium sensor (NCS) and neuronal calcium-binding protein (nCaBP) families consist of Ca(2+) sensors with largely unknown synaptic functions despite an increasing number of interaction partners. Particularly how these sensors operate in spines in the presence of CaM has not been discussed in detail before. The limited Ca(2+) resources and the existence of common targets create a highly competitive environment where Ca(2+) sensors compete with each other for Ca(2+) and target binding. In this review, we take a simple numerical approach to put forth possible scenarios and their impact on signaling via Ca(2+) sensors of the NCS and nCaBP families. We also discuss the ways in which spine geometry and properties of ion channels, their kinetics and distribution, alter the spatio-temporal aspects of Ca(2+) transients in dendritic spines, whose interplay with Ca(2+) sensors in turn influences the race for Ca(2+).
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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.