Evidence map›Paper›PMID 29339832›Full record

ArticleScientific reports2018

CLOCKΔ19 mutation modifies the manner of synchrony among oscillation neurons in the suprachiasmatic nucleus.

Mitsugu Sujino, Takeshi Asakawa, Mamoru Nagano, Satoshi Koinuma, Koh-Hei Masumoto, Yasufumi Shigeyoshi

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
0.7field-weighted citation impact, top 35% of its field
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

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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

6 citing papers in PubMed, 14 citations in OpenAlex.

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  6. Keeping time in the lamina terminalis: Novel oscillator properties of forebrain sensory circumventricular organs.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2020
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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 at 3 institutions in 1 country.

Mitsugu SujinoDepartment of Anatomy and Neurobiology, Kindai University School of Medicine 377-2 Ohno-Higashi, Osakasayama City, Osaka, 589-8511, Japan. sujino@med.kindai.ac.jp.
Takeshi AsakawaInformation Systems Center, University of Occupational and Environmental Health, 1-1, Iseigaoka, Yahatanishi-ku Kitakyushu-shi, Fukuoka, 807-8555, Japan.
Mamoru NaganoDepartment of Anatomy and Neurobiology, Kindai University School of Medicine 377-2 Ohno-Higashi, Osakasayama City, Osaka, 589-8511, Japan.
Satoshi KoinumaDepartment of Anatomy and Neurobiology, Kindai University School of Medicine 377-2 Ohno-Higashi, Osakasayama City, Osaka, 589-8511, Japan.
Koh-Hei MasumotoCenter for Medical Science, International University of Health and Welfare 2600-1 Kitakanemaru, Ohtawara, Tochigi, 324-8501, Japan.
Yasufumi ShigeyoshiDepartment of Anatomy and Neurobiology, Kindai University School of Medicine 377-2 Ohno-Higashi, Osakasayama City, Osaka, 589-8511, Japan. shigey@med.kindai.ac.jp.
Kindai University · JPInternational University of Health and Welfare · JPUniversity of Occupational and Environmental Health Japan · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

In mammals, the principal circadian oscillator exists in the hypothalamic suprachiasmatic nucleus (SCN). In the SCN, CLOCK works as an essential component of molecular circadian oscillation, and ClockΔ19 mutant mice show unique characteristics of circadian rhythms such as extended free running periods, amplitude attenuation, and high-magnitude phase-resetting responses. Here we investigated what modifications occur in the spatiotemporal organization of clock gene expression in the SCN of ClockΔ19 mutants. The cultured SCN, sampled from neonatal homozygous ClockΔ19 mice on an ICR strain comprising PERIOD2::LUCIFERASE, demonstrated that the Clock gene mutation not only extends the circadian period, but also affects the spatial phase and period distribution of circadian oscillations in the SCN. In addition, disruption of the synchronization among neurons markedly attenuated the amplitude of the circadian rhythm of individual oscillating neurons in the mutant SCN. Further, with numerical simulations based on the present studies, the findings suggested that, in the SCN of the ClockΔ19 mutant mice, stable oscillation was preserved by the interaction among oscillating neurons, and that the orderly phase and period distribution that makes a phase wave are dependent on the functionality of CLOCK.

Indexed as

AnimalsBehavior, AnimalCircadian RhythmCLOCK ProteinsCyclic AMPMaleMiceMice, Inbred C57BLMice, Inbred ICRModels, TheoreticalMutagenesisNeuronsPeriod Circadian ProteinsSignal TransductionSuprachiasmatic NucleusTetrodotoxinClock protein, mouseCLOCK ProteinsCyclic AMPPer2 protein, mousePeriod Circadian ProteinsTetrodotoxin

Identifiers

PMID29339832
PMCPMC5770461
OpenAlexW2783531066

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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.