Evidence map›Paper›PMID 20348918›Full record

ArticleNature neuroscience2010

Reduction in endocannabinoid tone is a homeostatic mechanism for specific inhibitory synapses.

Jimok Kim, Bradley E Alger

Open access · greenAbstract read
In one paragraph

Article in Nature neuroscience, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 94 papers.

0numbers the graph read from it
0cells of the map it votes in
94citing papers in PubMed
6.8field-weighted citation impact, top 2% 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

94 citing papers in PubMed, 150 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Role of the Endocannabinoid System in Fibromyalgia.Current issues in molecular biology · 2025
    Review
  6. Article
  7. Article
  8. Article
  9. Article
  10. Article
  11. Article
  12. Electrophysiology of Endocannabinoid Signaling.Methods in molecular biology (Clifton, N.J.) · 2023
    Article
  13. Endocannabinoids at the synapse and beyond: implications for neuropsychiatric disease pathophysiology and treatment.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2023
    Review
  14. Article
  15. Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. Article

34 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

2 authors at 1 institution in 1 country.

Jimok KimDepartments of Physiology, University of Maryland School of Medicine, Baltimore, Maryland, USA.
Bradley E Alger
University of Maryland, Baltimore · US

Funding

Endocannabinoids and GABAergic Control of PlasticityR01DA014625 · NIDA · UNIVERSITY OF MARYLAND BALTIMORE · PI ALGER, BRADLEY E · 2001 to 2011
$2.9M
Interactions Among Hippocampal Interneuron CircuitsR01MH077277 · NIMH · UNIVERSITY OF MARYLAND BALTIMORE · PI ALGER, BRADLEY E · 2006 to 2012
$1.8M
NIDA NIH HHS R01 DA014625NIMH NIH HHS R01 MH077277
6 · The paper itself

Abstract

When chronic alterations in neuronal activity occur, network gain is maintained by global homeostatic scaling of synaptic strength, but the stability of microcircuits can be controlled by unique adaptations that differ from the global changes. It is not understood how specificity of synaptic tuning is achieved. We found that, although a large population of inhibitory synapses was homeostatically scaled down after chronic inactivity, decreased endocannabinoid tone specifically strengthened a subset of GABAergic synapses that express cannabinoid receptors. In rat hippocampal slice cultures, a 3-5-d blockade of neuronal firing facilitated uptake and degradation of anandamide. The consequent reduction in basal stimulation of cannabinoid receptors augmented GABA release probability, fostering rapid depression of synaptic inhibition and on-demand disinhibition. This regulatory mechanism, mediated by activity-dependent changes in tonic endocannabinoid level, permits selective local tuning of inhibitory synapses in hippocampal networks.

Indexed as

EndocannabinoidsAgatoxinsAnimalsArachidonic AcidsBenzamidesBenzoxazinesBiophysicsCalciumCalcium Channel BlockersCannabinoid Receptor ModulatorsCarbamatesConotoxinsDose-Response Relationship, DrugDown-RegulationDrug InteractionsElectric Stimulation(3R)-((2,3-dihydro-5-methyl-3-((4-morpholinyl)methyl)pyrrolo-(1,2,3-de)-1,4-benzoxazin-6-yl)(1-naphthalenyl))methanoneagatoxin-489AgatoxinsAM 251anandamideArachidonic AcidsBenzamidesBenzoxazinesCalciumCalcium Channel BlockersCannabinoid Receptor ModulatorsCarbamatesConotoxinscyclohexyl carbamic acid 3'-carbamoylbiphenyl-3-yl esterEndocannabinoidsEnzyme InhibitorsExcitatory Amino Acid Antagonistsgamma-Aminobutyric AcidGlyceridesglyceryl 2-arachidonateMorpholinesN-(4-hydroxyphenyl)arachidonylamideNaphthalenesPiperidinesPolyaminesPolyunsaturated AlkamidesPyrazolesReceptor, Cannabinoid, CB1RimonabantSodium Channel BlockersTetrodotoxin

Identifiers

PMID20348918
PMCPMC2860695
OpenAlexW1979518536

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.