Evidence map›Paper›PMID 25888781›Full record

ArticleJournal of neuroinflammation2015

Calcium dysregulation via L-type voltage-dependent calcium channels and ryanodine receptors underlies memory deficits and synaptic dysfunction during chronic neuroinflammation.

Sarah C Hopp, Heather M D'Angelo, Sarah E Royer, Roxanne M Kaercher, Alexis M Crockett, Linda Adzovic, Gary L Wenk

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
1.9field-weighted citation impact, top 15% 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

27 citing papers in PubMed, 50 citations in OpenAlex.

  1. Trial
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  9. Review
  10. Astrocytes Reduce Store-Operated CaPharmaceuticals (Basel, Switzerland) · 2022
    Article
  11. L-Type CaInternational journal of molecular sciences · 2022
    Article
  12. Article
  13. Article
  14. Article
  15. Review
  16. Review
  17. Article
  18. Presynaptic L-Type CaThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2020
    Article
  19. Review
  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

7 authors at 1 institution in 1 country.

Sarah C HoppDepartments of Neuroscience, Ohio State University, Columbus, OH, 43210, USA. hopp.8@osu.edu.
Heather M D'AngeloDepartment of Psychology, Ohio State University, 1835 Neil Ave, Columbus, OH, 43210, USA. dangelo.42@osu.edu.
Sarah E RoyerDepartments of Neuroscience, Ohio State University, Columbus, OH, 43210, USA. royer.49@osu.edu.
Roxanne M KaercherDepartment of Psychology, Ohio State University, 1835 Neil Ave, Columbus, OH, 43210, USA. Kaercher.7@osu.edu.
Alexis M CrockettDepartments of Neuroscience, Ohio State University, Columbus, OH, 43210, USA. crockett.111@osu.edu.
Linda AdzovicDepartment of Psychology, Ohio State University, 1835 Neil Ave, Columbus, OH, 43210, USA. Adzovic.1@osu.edu.
Gary L WenkDepartments of Neuroscience, Ohio State University, Columbus, OH, 43210, USA. wenk.6@osu.edu.
The Ohio State University · US

Funding

Vulnerability to neuroinflammation of brainstem ascending aminergic systemsR01AG037320 · NIA · OHIO STATE UNIVERSITY · PI WENK, GARY L. · 2011 to 2015
$1.5M
Aging microglia-neuronal communicationR01AG030331 · NIA · OHIO STATE UNIVERSITY · PI WENK, GARY L. · 2008 to 2012
$1.3M
Howard Hughes Medical InstituteNIA NIH HHS R01 AG030331NIA NIH HHS R01 AG037320
6 · The paper itself

Abstract

backgroundChronic neuroinflammation and calcium (Ca(+2)) dysregulation are both components of Alzheimer's disease. Prolonged neuroinflammation produces elevation of pro-inflammatory cytokines and reactive oxygen species which can alter neuronal Ca(+2) homeostasis via L-type voltage-dependent Ca(+2) channels (L-VDCCs) and ryanodine receptors (RyRs). Chronic neuroinflammation also leads to deficits in spatial memory, which may be related to Ca(+2) dysregulation.

methodsThe studies herein use an in vivo model of chronic neuroinflammation: rats were infused intraventricularly with a continuous small dose of lipopolysaccharide (LPS) or artificial cerebrospinal fluid (aCSF) for 28 days. The rats were treated with the L-VDCC antagonist nimodipine or the RyR antagonist dantrolene.

resultsLPS-infused rats had significant memory deficits in the Morris water maze, and this deficit was ameliorated by treatment with nimodipine. Synaptosomes from LPS-infused rats had increased Ca(+2) uptake, which was reduced by a blockade of L-VDCCs either in vivo or ex vivo.

conclusionsTaken together, these data indicate that Ca(+2) dysregulation during chronic neuroinflammation is partially dependent on increases in L-VDCC function. However, blockade of the RyRs also slightly improved spatial memory of the LPS-infused rats, demonstrating that other Ca(+2) channels are dysregulated during chronic neuroinflammation. Ca(+2)-dependent immediate early gene expression was reduced in LPS-infused rats treated with dantrolene or nimodipine, indicating normalized synaptic function that may underlie improvements in spatial memory. Pro-inflammatory markers are also reduced in LPS-infused rats treated with either drug. Overall, these data suggest that Ca(+2) dysregulation via L-VDCCs and RyRs play a crucial role in memory deficits resulting from chronic neuroinflammation.

Indexed as

AIDS-Related ComplexAnalysis of VarianceAnimalsCalciumCalcium Channel BlockersCalcium Channels, L-TypeChronic DiseaseDantroleneDisease Models, AnimalEncephalitisGene Expression RegulationLipopolysaccharidesMaze LearningMemory DisordersMuscle Relaxants, CentralNimodipineCalciumCalcium Channel BlockersCalcium Channels, L-TypeDantroleneLipopolysaccharidesMuscle Relaxants, CentralNimodipineRyanodine Receptor Calcium Release Channel

Identifiers

PMID25888781
PMCPMC4377218
OpenAlexW2066165879

What OpenQuestion holds

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LicenceCC BY
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.