Evidence map›Paper›PMID 28178527›Full record

ArticleCell reports2017

An Intrinsic Transcriptional Program Underlying Synaptic Scaling during Activity Suppression.

Katie Schaukowitch, Austin L Reese, Seung-Kyoon Kim, Gokhul Kilaru, Jae-Yeol Joo, Ege T Kavalali, Tae-Kyung Kim

Abstract read
In one paragraph

Article in Cell reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.

0numbers the graph read from it
0cells of the map it votes in
50citing 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

50 citing papers in PubMed.

  1. Hyper-maturity and accelerated aging in the hippocampus of mouse models of neuropsychiatric disorders with anxiety-like behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Article
  3. Article
  4. Activity Deprivation Modulates the Shank3/Homer1/mGluR5 Signaling Pathway to Enable Synaptic Upscaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025
    Article
  5. Review
  6. Article
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  8. Modular arrangement of synaptic and intrinsic homeostatic plasticity within visual cortical circuits.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
  9. Article
  10. Article
  11. Article
  12. Article
  13. Article
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  18. Review
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  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.

Katie SchaukowitchDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.
Austin L ReeseDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.
Seung-Kyoon KimDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.
Gokhul KilaruDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.
Jae-Yeol JooDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.
Ege T KavalaliDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA.
Tae-Kyung KimDepartment of Neuroscience, University of Texas Southwestern Medical Center, Dallas, TX 75390-9111, USA. Electronic address: taekyung.kim@utsouthwestern.edu.

Funding

Role of SNARE Interactions in Central Synapse FunctionR01MH066198 · NIMH · VANDERBILT UNIVERSITY · PI KAVALALI, EGE T · 2004 to 2023
$7.9M
Basic Science Training Program in the Neurobiology of Mental IllnessT32MH076690 · NIMH · UT SOUTHWESTERN MEDICAL CENTER · PI TAMMINGA, CAROL A · 2007 to 2017
$2.3M
The epigenetic mechanism of enhancer RNA in behavioral plasticityR01NS085418 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI KIM, TAE-KYUNG · 2013 to 2017
$1.7M
The Cellular Biophysics of the Neuron Training ProgramT32NS069562 · NINDS · UT SOUTHWESTERN MEDICAL CENTER · PI KAVALALI, EGE T · 2010 to 2014
$568k
NIMH NIH HHS R01 MH066198NIMH NIH HHS T32 MH076690NINDS NIH HHS R01 NS085418NINDS NIH HHS T32 NS069562
6 · The paper itself

Abstract

Homeostatic scaling allows neurons to maintain stable activity patterns by globally altering their synaptic strength in response to changing activity levels. Suppression of activity by the blocking of action potentials increases synaptic strength through an upregulation of surface α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors. Although this synaptic upscaling was shown to require transcription, the molecular nature of the intrinsic transcription program underlying this process and its functional significance have been unclear. Using RNA-seq, we identified 73 genes that were specifically upregulated in response to activity suppression. In particular, Neuronal pentraxin-1 (Nptx1) increased within 6 hr of activity blockade, and knockdown of this gene blocked the increase in synaptic strength. Nptx1 induction is mediated by calcium influx through the T-type voltage-gated calcium channel, as well as two transcription factors, SRF and ELK1. Altogether, these results uncover a transcriptional program that specifically operates when neuronal activity is suppressed to globally coordinate the increase in synaptic strength.

Indexed as

Action PotentialsAnimalsCalciumCalcium Channels, T-TypeCells, CulturedExcitatory Postsynaptic PotentialsHomeostasisMiceNerve Tissue ProteinsNeuronal PlasticityNeuronsReceptors, AMPASynapsesTranscription FactorsTranscription, GeneticUp-RegulationCalciumCalcium Channels, T-TypeNerve Tissue ProteinsReceptors, AMPATranscription Factorsenhancerhomeostatic scalingNptx1transcriptionT-VGCC

Identifiers

PMID28178527
PMCPMC5524384

What OpenQuestion holds

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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.