ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Ca2+ sparks and puffs are generated and interact in rat hippocampal CA1 pyramidal neuron dendrites.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Calmodulin controls spatial and temporal specificity of calcium-induced calcium release.PLoS computational biology · 2026Article
- Endoplasmic Reticulum Calcium Signaling in Hippocampal Neurons.Biomolecules · 2024Review
- Nano-organization of synaptic calcium signaling.Biochemical Society transactions · 2024Review
- Axonal ER CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2023Article
- Endoplasmic Reticulum-Plasma Membrane Junctions as Sites of Depolarization-Induced CaAnnual review of physiology · 2023Review
- Neuronal microRNAs safeguard ER CaCellular and molecular life sciences : CMLS · 2022Article
- Role of the endoplasmic reticulum in synaptic transmission.Current opinion in neurobiology · 2022Review
- Subcellular localization of hippocampal ryanodine receptor 2 and its role in neuronal excitability and memory.Communications biology · 2022Article
- The spatio-temporal properties of calcium transients in hippocampal pyramidal neuronsFrontiers in cellular neuroscience · 2022Article
- Population imaging discrepancies between a genetically-encoded calcium indicator (GECI) versus a genetically-encoded voltage indicator (GEVI).Scientific reports · 2021Article
- The Molecular Basis for the Calcium-Dependent Slow Afterhyperpolarization in CA1 Hippocampal Pyramidal Neurons.Frontiers in physiology · 2021Review
- Article
- Stores, Channels, Glue, and Trees: Active Glial and Active Dendritic Physiology.Molecular neurobiology · 2019Review
- Cellular information dynamics through transmembrane flow of ions.Scientific reports · 2017Article
- Determining the Roles of Inositol Trisphosphate Receptors in Neurodegeneration: Interdisciplinary Perspectives on a Complex Topic.Molecular neurobiology · 2017Review
- SamuROI, a Python-Based Software Tool for Visualization and Analysis of Dynamic Time Series Imaging at Multiple Spatial Scales.Frontiers in neuroinformatics · 2017Article
- Imaging with organic indicators and high-speed charge-coupled device cameras in neurons: some applications where these classic techniques have advantages.Neurophotonics · 2015Review
- Dendritic calcium nonlinearities switch the direction of synaptic plasticity in fast-spiking interneurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2014Article
- Calcium Sparks in the Heart: Dynamics and Regulation.Research and reports in biologyArticle
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Authors and funding
2 authors.
Funding
Abstract
1,4,5-Inositol trisphosphate receptors (IP3Rs) and ryanodine receptors (RyRs) mediate release of Ca(2+) from internal stores in many neurons. The details of the spatial and temporal characteristics of these signals and their interactions in dendrites remain to be clarified. We found that localized Ca(2+) release events, with no associated change in membrane potential, occurred spontaneously in the dendrites of rat hippocampal CA1 pyramidal neurons. Their rate, but not their amplitude or time course, could be modulated by changes in membrane potential. Together, these results suggest that the spontaneous events are similar to RyR-dependent Ca(2+) "sparks" found in cardiac myocytes. In addition, we found that we could generate another kind of localized Ca(2+) release event by either a synaptic tetanus in the presence of 3-((R)-2-carboxypiperazine-4-yl)-propyl-1-phosphonic acid and CNQX or by uncaging IP3. These events had slower rise times and decay times than sparks and were more heterogeneous. These properties are similar to Ca(2+) "puffs" found in oocytes. These two localized signals interact. Low-intensity tetanic synaptic stimulation or uncaging of IP3 increased the decay time of spontaneous Ca(2+) events without changing their rise time or amplitude. Pharmacological experiments suggest that this event widening is attributable to a delayed IP3R-mediated release of Ca(2+) triggered by the synergistic action of IP3 and Ca(2+) released by RyRs. The actions of IP3 appear to be confined to the main apical dendrite because uncaging IP3 in the oblique dendrites has no effect on the time course of localized events or backpropagating action potential-evoked Ca(2+) signals in this region.
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