ArticleFrontiers in cellular neuroscience2019
Functional Coupling of Cav2.3 and BK Potassium Channels Regulates Action Potential Repolarization and Short-Term Plasticity in the Mouse Hippocampus.
Article in Frontiers in cellular neuroscience, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 20 citations in OpenAlex.
- Characterization of Three Distinct Loss-of-Function Cav2.3 Variants.International journal of molecular sciences · 2026Article
- Large conductance voltage-and calcium-activated KFrontiers in pharmacology · 2024Review
- CaInternational journal of molecular sciences · 2023Review
- An unbiased algorithm for objective separation of Alzheimer's, Alzheimer's mixed with cerebrovascular symptomology, and healthy controls from one another using electrovestibulography (EVestG).Medical & biological engineering & computing · 2022Article
- Ion Channel Partnerships: Odd and Not-So-Odd Couples Controlling Neuronal Ion Channel Function.International journal of molecular sciences · 2022Review
- R-type voltage-gated CaCell reports · 2022Article
- BK Channel Regulation of Afterpotentials and Burst Firing in Cerebellar Purkinje Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Structural and Functional Coupling of Calcium-Activated BK Channels and Calcium-Permeable Channels Within Nanodomain Signaling Complexes.Frontiers in physiology · 2021Review
- BK Channels Are Activated by Functional Coupling With L-Type CaFrontiers in insect science · 2021Article
- Altered Expression of Ion Channels in White Matter Lesions of Progressive Multiple Sclerosis: What Do We Know About Their Function?Frontiers in cellular neuroscience · 2021Review
- Cav2.3 channels contribute to dopaminergic neuron loss in a model of Parkinson's disease.Nature communications · 2019Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Voltage-gated ion channels are essential for signal generation and propagation in neurons and other excitable cells. The high-voltage activated calcium-channel Cav2.3 is expressed throughout the central and peripheral nervous system, and within CA1 hippocampal pyramidal neurons it is localized throughout the somato-dendritic region and dendritic spines. Cav2.3 has been shown to provide calcium for other calcium-dependent potassium channels including small-conductance calcium-activated potassium channels (SK), but big-conductance calcium-activated potassium channels (BK) have been thought to be activated by calcium from all known voltage-gated calcium channels, except Cav2.3. Here we show for the first time that CA1 pyramidal cells which lack Cav2.3 show altered action potential (AP) waveforms, which can be traced back to reduced SK- and BK-channel function. This change in AP waveform leads to strengthened synaptic transmission between CA1 and the subiculum, resulting in increased short-term plasticity. Our results demonstrate that Cav2.3 impacts cellular excitability through functional interaction with BK channels, impacting communication between hippocampal subregions.
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Registered trials
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