ArticleSleep2014
The CaV2.3 R-type voltage-gated Ca2+ channel in mouse sleep architecture.
Article in Sleep, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 21 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
21 citing papers in PubMed, 32 citations in OpenAlex.
- Trial
- Sleep prevents brain phosphoproteome disruption to safeguard survival.Cell discovery · 2025Article
- Role of Ion Channels in Alzheimer's Disease Pathophysiology.The Journal of membrane biology · 2025Review
- CaScientific reports · 2025Article
- Voltage Gated Ion Channels and Sleep.The Journal of membrane biology · 2024Review
- A novel role for phospholamban in the thalamic reticular nucleus.Scientific reports · 2024Article
- Role of Cav2.3 (R-type) Calcium Channel in Pain and Analgesia: A Scoping Review.Current neuropharmacology · 2024Article
- Further Evidence that Inhibition of Neuronal Voltage-Gated Calcium Channels Contributes to the Hypnotic Effect of Neurosteroid Analogue, 3β-OH.Frontiers in pharmacology · 2022Article
- Breeding of CaScientific reports · 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
- Genetic Associations between Voltage-Gated Calcium Channels and Psychiatric Disorders.International journal of molecular sciences · 2019Review
- Gender specific click and tone burst evoked ABR datasets from mice lacking the CaData in brief · 2018Article
- Article
- In vitro and in vivo phosphorylation of the CaChannels (Austin, Tex.) · 2018Review
- Gender specific hippocampal whole genome transcriptome data from mice lacking the CaData in brief · 2017Article
- The thalamic mGluR1-PLCβ4 pathway is critical in sleep architecture.Molecular brain · 2016Article
- Review: CaThe open neurology journal · 2016Article
- EEG Radiotelemetry in Small Laboratory Rodents: A Powerful State-of-the Art Approach in Neuropsychiatric, Neurodegenerative, and Epilepsy Research.Neural plasticity · 2016Review
- A scientific assessment of CaV2.3 voltage-gated Ca2+ channels in rodent sleep architecture.Sleep · 2015Article
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
STUDY
objectivesVoltage-gated Ca(2+) channels (VGCCs) are key elements in mediating thalamocortical rhythmicity. Low-voltage activated (LVA) CaV 3 T-type Ca(2+) channels have been related to thalamic rebound burst firing and to generation of non-rapid eye movement (NREM) sleep. High-voltage activated (HVA) CaV 1 L-type Ca(2+) channels, on the opposite, favor the tonic mode of action associated with higher levels of vigilance. However, the role of the HVA Non-L-type CaV2.3 Ca(2+) channels, which are predominantly expressed in the reticular thalamic nucleus (RTN), still remains unclear. Recently, CaV2.3(-/-) mice were reported to exhibit altered spike-wave discharge (SWD)/absence seizure susceptibility supported by the observation that CaV2.3 mediated Ca(2+) influx into RTN neurons can trigger small-conductance Ca(2+)-activated K(+)-channel type 2 (SK2) currents capable of maintaining thalamic burst activity. Based on these studies we investigated the role of CaV2.3 R-type Ca(2+) channels in rodent sleep.
methodsThe role of CaV2.3 Ca(2+) channels was analyzed in CaV2.3(-/-) mice and controls in both spontaneous and artificial urethane-induced sleep, using implantable video-EEG radiotelemetry. Data were analyzed for alterations in sleep architecture using sleep staging software and time-frequency analysis.
resultsCaV2.3 deficient mice exhibited reduced wake duration and increased slow-wave sleep (SWS). Whereas mean sleep stage durations remained unchanged, the total number of SWS epochs was increased in CaV2.3(-/-) mice. Additional changes were observed for sleep stage transitions and EEG amplitudes. Furthermore, urethane-induced SWS mimicked spontaneous sleep results obtained from CaV2.3 deficient mice. Quantitative Real-time PCR did not reveal changes in thalamic CaV3 T-type Ca(2+) channel expression. The detailed mechanisms of SWS increase in CaV2.3(-/-) mice remain to be determined.
conclusionsLow-voltage activated CaV2.3 R-type Ca(2+) channels in the thalamocortical loop and extra-thalamocortical circuitries substantially regulate rodent sleep architecture thus representing a novel potential target for pharmacological treatment of sleep disorders in the future.
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