Evidence map›Paper›PMID 22159093›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011

Decrease in calcium concentration triggers neuronal retinoic acid synthesis during homeostatic synaptic plasticity.

Hui-Li Wang, Zhenjie Zhang, Maik Hintze, Lu Chen

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 68 papers.

0numbers the graph read from it
0cells of the map it votes in
68citing papers in PubMed
3.2field-weighted citation impact, top 7% 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

68 citing papers in PubMed, 104 citations in OpenAlex.

  1. Acetazolamide inhibition of carbonic anhydrase 4 reverses opioid-induced synaptic rearrangements in nucleus accumbens and reduces drug-seeking behavior.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
    Article
  2. Article
  3. Frontiers in cellular neuroscience · 2026
    Review
  4. Article
  5. Article
  6. Review
  7. Review
  8. Article
  9. Article
  10. Review
  11. Article
  12. Rapid homeostatic plasticity and neuropsychiatric therapeutics.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Review
  13. Article
  14. Article
  15. Inactivity and CaScientific reports · 2022
    Article
  16. Activity-dependent modulation of neuronal KThe Journal of biological chemistry · 2022
    Article
  17. Review
  18. Article
  19. Article
  20. From mice to men.eLife · 2021
    Article

8 more citing papers are in PubMed but not listed here.

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

4 authors at 1 institution in 2 countries.

Hui-Li WangStanford Institute of Neuro-Innovation and Translational Neuroscience and Department of Psychiatry and Behavioral Sciences, Stanford University School of Medicine, Stanford, California 94305-5453, USA.
Zhenjie Zhang
Maik Hintze
Lu Chen
Hefei University of Technology · CN

Funding

Role of synaptotagmins and neurexin ligands in homeostatic synaptic plasticityP50MH086403 · NIMH · STANFORD UNIVERSITY · PI DEISSEROTH, KARL A. · 2009 to 2019
$18.4M
Regulation of synaptic transmission by retinoic acid signalingR01MH091193 · NIMH · STANFORD UNIVERSITY · PI CHEN, LU · 2011 to 2015
$2.3M
NIMH NIH HHS 1P50MH86403NIMH NIH HHS 1R01MH091193NIMH NIH HHS P50 MH086403NIMH NIH HHS R01 MH091193
6 · The paper itself

Abstract

Blockade of synaptic activity induces homeostatic plasticity, in part by stimulating synthesis of all-trans retinoic acid (RA), which in turn increases AMPA receptor synthesis. However, the synaptic signal that triggers RA synthesis remained unknown. Using multiple activity-blockade protocols that induce homeostatic synaptic plasticity, here we show that RA synthesis is activated whenever postsynaptic Ca(2+) entry is significantly decreased and that RA is required for upregulation of synaptic strength under these homeostatic plasticity conditions, suggesting that Ca(2+) plays an inhibitory role in RA synthesis. Consistent with this notion, we demonstrate that both transient Ca(2+) depletion by membrane-permeable Ca(2+) chelators and chronic blockage of L-type Ca(2+)-channels induces RA synthesis. Moreover, the source of dendritic Ca(2+) entry that regulates RA synthesis is not specific because mild depolarization with KCl is sufficient to reverse synaptic scaling induced by L-type Ca(2+)-channel blocker. By expression of a dihydropyridine-insensitive L-type Ca(2+) channel, we further show that RA acts cell autonomously to modulate synaptic transmission. Our findings suggest that, in synaptically active neurons, modest "basal" levels of postsynaptic Ca(2+) physiologically suppress RA synthesis, whereas in synaptically inactive neurons, decreases in the resting Ca(2+) levels induce homeostatic plasticity by stimulating synthesis of RA that then acts in a cell-autonomous manner to increase AMPA receptor function.

Indexed as

AnimalsCalciumCells, CulturedDendritesDihydropyridinesEmbryo, MammalianExcitatory Amino Acid AntagonistsGreen Fluorescent ProteinsHippocampusHomeostasisNeuronal PlasticityNeuronsPatch-Clamp TechniquesRatsSodium Channel BlockersTetrodotoxinCalciumDihydropyridinesenhanced green fluorescent proteinExcitatory Amino Acid AntagonistsGreen Fluorescent ProteinsSodium Channel BlockersTetrodotoxinTretinoin

Identifiers

PMID22159093
PMCPMC3457695
OpenAlexW2003137201

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.