Evidence map›Paper›PMID 29996097›Full record

ArticleCell reports2018

Aberrant Calcium Signaling in Astrocytes Inhibits Neuronal Excitability in a Human Down Syndrome Stem Cell Model.

Grace O Mizuno, Yinxue Wang, Guilai Shi, Yizhi Wang, Junqing Sun, Stelios Papadopoulos, Gerard J Broussard, Elizabeth K Unger, Wenbin Deng, Jason Weick and 5 more

Abstract read
In one paragraph

Article in Cell reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed, 1 pooled it
–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

37 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
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  19. Control of complex behavior by astrocytes and microglia.Neuroscience and biobehavioral reviews · 2022
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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

15 authors.

Grace O MizunoDepartment of Biochemistry and Molecular Medicine, Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, CA, USA.
Yinxue WangBradley Department of Electrical and Computer Engineering, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
Guilai ShiDepartment of Biochemistry and Molecular Medicine, Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, CA, USA.
Yizhi WangBradley Department of Electrical and Computer Engineering, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
Junqing SunDepartment of Pharmacology, University of California, Davis, Davis, CA, USA.
Stelios PapadopoulosDepartment of Biochemistry and Molecular Medicine, Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, CA, USA.
Gerard J BroussardDepartment of Biochemistry and Molecular Medicine, Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, CA, USA.
Elizabeth K UngerDepartment of Biochemistry and Molecular Medicine, Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, CA, USA.
Wenbin DengDepartment of Biochemistry and Molecular Medicine, Shriner's Hospital, University of California, Davis, Davis, CA, USA.
Jason WeickDepartment of Neuroscience, University of New Mexico, Albuquerque, NM, USA.
Anita BhattacharyyaWaisman Center, University of Wisconsin, Madison, Madison, WI, USA.
Chao-Yin ChenDepartment of Pharmacology, University of California, Davis, Davis, CA, USA.
Guoqiang YuBradley Department of Electrical and Computer Engineering, Virginia Polytechnic Institute and State University, Blacksburg, VA, USA.
Loren L LoogerJanelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA, USA.
Lin TianDepartment of Biochemistry and Molecular Medicine, Department of Psychiatry and Behavioral Sciences, University of California, Davis, Davis, CA, USA. Electronic address: lintian@ucdavis.edu.

Funding

University of New Mexico (UNM) Center for Brain Recovery and RepairP20GM109089 · NIGMS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI SHUTTLEWORTH, CLAUDE W · 2015 to 2024
$22.7M
Decoding Astrocyte Signaling in Neural Circuitry with Novel Computational Modeling and Analytical ToolsR01MH110504 · NIMH · VIRGINIA POLYTECHNIC INST AND ST UNIV · PI YUE WANG · 2017 to 2026
$6.1M
Genetically encoded indicators for large-scale sensing of neuromodulatory signaling in behaving animalsU01NS103522 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI NIMMERJAHN, AXEL, TIAN, LIN · 2017 to 2019
$2.9M
Fluorescent biosensors for imaging neurotransmitters: observing synapses in actioDP2MH107056 · NIMH · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TIAN, LIN · 2014 to 2014
$2.3M
Genetically encoded sensors for the biogenic amine: watching neuromodulation in actionU01NS090604 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI TIAN, LIN · 2014 to 2016
$1.3M
Opioid Sensitive GABA inputs to the Ventral MidbrainR01DA034388 · NIDA · OREGON HEALTH & SCIENCE UNIVERSITY · PI WILLIAMS, JOHN T · 2012 to 2016
$967k
Microsystems for Modeling Neurodevelopmental DisordersR21NS095325 · NINDS · UNIVERSITY OF CALIFORNIA AT DAVIS · PI REVZIN, ALEXANDER, TIAN, LIN · 2016 to 2017
$418k
Light-based regulation of autophagy processing to target pathological forms of tauR21NS093442 · NINDS · UNIVERSITY OF NEW MEXICO HEALTH SCIS CTR · PI BHASKAR, KIRAN, WEICK, JASON P · 2016 to 2017
$417k
Astrocytes in Down Syndrome SynaptogenesisR03HD064880 · NICHD · UNIVERSITY OF WISCONSIN-MADISON · PI BHATTACHARYYA, ANITA · 2010 to 2010
$74k
NICHD NIH HHS R03 HD064880NIDA NIH HHS R01 DA034388NIGMS NIH HHS P20 GM109089NIMH NIH HHS DP2 MH107056NIMH NIH HHS R01 MH110504NINDS NIH HHS R21 NS093442NINDS NIH HHS R21 NS095325NINDS NIH HHS U01 NS090604NINDS NIH HHS U01 NS103522
6 · The paper itself

Abstract

Down syndrome (DS) is a genetic disorder that causes cognitive impairment. The staggering effects associated with an extra copy of human chromosome 21 (HSA21) complicates mechanistic understanding of DS pathophysiology. We examined the neuron-astrocyte interplay in a fully recapitulated HSA21 trisomy cellular model differentiated from DS-patient-derived induced pluripotent stem cells (iPSCs). By combining calcium imaging with genetic approaches, we discovered the functional defects of DS astroglia and their effects on neuronal excitability. Compared with control isogenic astroglia, DS astroglia exhibited more-frequent spontaneous calcium fluctuations, which reduced the excitability of co-cultured neurons. Furthermore, suppressed neuronal activity could be rescued by abolishing astrocytic spontaneous calcium activity either chemically by blocking adenosine-mediated signaling or genetically by knockdown of inositol triphosphate (IP

Indexed as

Calcium SignalingModels, BiologicalAnimalsAstrocytesCalciumCell DifferentiationDown SyndromeEndoplasmic ReticulumHumansImaging, Three-DimensionalInduced Pluripotent Stem CellsInositol 1,4,5-Trisphosphate ReceptorsNeuronsS100 ProteinsSynapsesCalciumInositol 1,4,5-Trisphosphate ReceptorsS100 Proteinsastrocyte-neuron interactionastrocytescalcium imagingDown syndromehuman IPSCsS100B

Identifiers

PMID29996097
PMCPMC6631348

What OpenQuestion holds

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LicenceCC BY-NC-ND
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.