Evidence map›Paper›PMID 25845695›Full record

ArticleSleep2015

Cacna1c (Cav1.2) Modulates Electroencephalographic Rhythm and Rapid Eye Movement Sleep Recovery.

Deependra Kumar, Nina Dedic, Cornelia Flachskamm, Stephanie Voulé, Jan M Deussing, Mayumi Kimura

Abstract read
In one paragraph

Article in Sleep, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

20 citing papers in PubMed.

  1. Article
  2. Voltage Gated Ion Channels and Sleep.The Journal of membrane biology · 2024
    Review
  3. Critical periods and Autism Spectrum Disorders, a role for sleep.Neurobiology of sleep and circadian rhythms · 2023
    Article
  4. The role of calcium and CaMKII in sleep.Frontiers in systems neuroscience · 2022
    Review
  5. Review
  6. Review
  7. Article
  8. Article
  9. Review
  10. Brief Report: A Gene Enrichment Approach Applied to Sleep and Autism.Journal of autism and developmental disorders · 2020
    Article
  11. Sleep as a translationally-relevant endpoint in studies of autism spectrum disorder (ASD).Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2020
    Review
  12. Article
  13. Article
  14. Article
  15. Restoring Serotonergic Homeostasis in the Lateral Hypothalamus Rescues Sleep Disturbances Induced by Early-Life Obesity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  16. Toward the Language Oscillogenome.Frontiers in psychology · 2018
    Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

6 authors.

Deependra KumarMax Planck Institute of Psychiatry, Munich, Germany.
Nina DedicMax Planck Institute of Psychiatry, Munich, Germany.
Cornelia FlachskammMax Planck Institute of Psychiatry, Munich, Germany.
Stephanie VouléMax Planck Institute of Psychiatry, Munich, Germany.
Jan M DeussingMax Planck Institute of Psychiatry, Munich, Germany.
Mayumi KimuraMax Planck Institute of Psychiatry, Munich, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

STUDY

objectivesThe CACNA1C gene encodes the alpha 1C (α1C) subunit of the Cav1.2 voltage-dependent L-type calcium channel (LTCC). Some of the other voltage-dependent calcium channels, e.g., P-/Q-type, Cav2.1; N-type, Cav2.2; E-/R-type, Cav2.3; and T-type, Cav3.3 have been implicated in sleep modulation. However, the contribution of LTCCs to sleep remains largely unknown. Based on recent genome-wide association studies, CACNA1C emerged as one of potential candidate genes associated with both sleep and psychiatric disorders. Indeed, most patients with mental illnesses have sleep problems and vice versa.

designTo investigate an impact of Cav1.2 on sleep-wake behavior and electroencephalogram (EEG) activity, polysomnography was performed in heterozygous Cacna1c (HET) knockout mice and their wild-type (WT) littermates under baseline and challenging conditions (acute sleep deprivation and restraint stress). MEASUREMENTS AND

resultsHET mice displayed significantly lower EEG spectral power than WT mice across high frequency ranges (beta to gamma) during wake and rapid eye movement (REM) sleep. Although HET mice spent slightly more time asleep in the dark period, daily amounts of sleep did not differ between the two genotypes. However, recovery sleep after exposure to both types of challenging stress conditions differed markedly; HET mice exhibited reduced REM sleep recovery responses compared to WT mice.

conclusionsThese results suggest the involvement of Cacna1c (Cav1.2) in fast electroencephalogram oscillations and REM sleep regulatory processes. Lower spectral gamma activity, slightly increased sleep demands, and altered REM sleep responses found in heterozygous Cacna1c knockout mice may rather resemble a sleep phenotype observed in schizophrenia patients.

Indexed as

ElectroencephalographyAnimalsCalcium Channels, L-TypeGamma RhythmHeterozygoteMaleMiceMice, KnockoutPolysomnographyRestraint, PhysicalSleep DeprivationSleep, REMWakefulnessCACNA1C protein, mouseCalcium Channels, L-TypeCacna1cCav1.2EEG spectral powerL-type voltage-dependent calcium channelschizophreniasleep

Identifiers

PMID25845695
PMCPMC4531405

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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.