Evidence map›Paper›PMID 30168855›Full record

ArticleJournal of neuroscience research2018

Pathophysiology in the suprachiasmatic nucleus in mouse models of Huntington's disease.

Dika Kuljis, Takashi Kudo, Yu Tahara, Cristina A Ghiani, Christopher S Colwell

Open access · greenAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroscience research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.2field-weighted citation impact, top 24% 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

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

17 citing papers in PubMed, 24 citations in OpenAlex.

  1. Review
  2. Review
  3. Review
  4. Article
  5. Article
  6. Article
  7. Restoration of Sleep and Circadian Behavior by Autophagy Modulation in Huntington's Disease.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    Article
  8. Review
  9. Review
  10. Circadian rhythms in neurodegenerative disorders.Nature reviews. Neurology · 2022
    Review
  11. Review
  12. Article
  13. Article
  14. Review
  15. Article
  16. Neurophysiological and Behavioral Effects of Anti-Orexinergic Treatments in a Mouse Model of Huntington's Disease.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019
    Article
  17. Review
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

5 authors at 2 institutions in 2 countries.

Dika KuljisDepartment of Neurobiology, University of California Los Angeles, Los Angeles, California.
Takashi KudoDepartment of Psychiatry & Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California.
Yu TaharaDepartment of Psychiatry & Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California.
Cristina A GhianiDepartment of Psychiatry & Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California.ORCID 0000-0002-9867-6185
Christopher S ColwellDepartment of Psychiatry & Biobehavioral Sciences, University of California Los Angeles, Los Angeles, California.ORCID 0000-0002-1059-184X
University of California, Los Angeles · USOkinawa Institute of Science and Technology Graduate University · JP

Funding

Neuroendocrinology, Sex Differences, and ReproductionT32HD007228 · NICHD · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI ARNOLD, ARTHUR P · 1985 to 2015
$3.9M
Time restricted feeding rescues circadian and motor dysfunction in a mouse model of Huntington's diseaseR21NS115041 · NINDS · UNIVERSITY OF CALIFORNIA LOS ANGELES · PI COLWELL, CHRISTOPHER SCOTT, PAUL, KETEMA N · 2020 to 2021
$547k
NICHD NIH HHS T32 HD007228NICHD NIH HHS T32 HD 07228-26NINDS NIH HHS R21 NS115041
6 · The paper itself

Abstract

Disturbances in sleep/wake cycle are a common complaint of individuals with Huntington's disease (HD) and are displayed by HD mouse models. The underlying mechanisms, including the possible role of the circadian timing system, are not well established. The BACHD mouse model of HD exhibits disrupted behavioral and physiological rhythms, including decreased electrical activity in the central circadian clock (suprachiasmatic nucleus, SCN). In this study, electrophysiological techniques were used to explore the ionic underpinning of the reduced spontaneous neural activity in male mice. We found that SCN neural activity rhythms were lost early in the disease progression and was accompanied by loss of the normal daily variation in resting membrane potential in the mutant SCN neurons. The low neural activity could be transiently reversed by direct current injection or application of exogenous N-methyl-d-aspartate (NMDA) thus demonstrating that the neurons have the capacity to discharge at WT levels. Exploring the potassium currents known to regulate the electrical activity of SCN neurons, our most striking finding was that these cells in the mutants exhibited an enhancement in the large-conductance calcium activated K

Indexed as

Action PotentialsAnimalsCircadian ClocksDisease Models, AnimalGABA-A Receptor AntagonistsHuntington DiseaseLarge-Conductance Calcium-Activated Potassium ChannelsMaleMembrane PotentialsMiceMice, TransgenicNeuronsPatch-Clamp TechniquesPyridazinesSuprachiasmatic NucleusGABA-A Receptor AntagonistsgabazineLarge-Conductance Calcium-Activated Potassium ChannelsPyridazinesBACHDBK currentcircadian rhythmsHuntington’s diseaseQ175suprachiasmatic nucleus

Identifiers

PMID30168855
PMCPMC7105277
OpenAlexW2889101774

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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.