Evidence map›Paper›PMID 18632563›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2008

Interneuron activity controls endocannabinoid-mediated presynaptic plasticity through calcineurin.

Boris D Heifets, Vivien Chevaleyre, Pablo E Castillo

Open access · greenAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 70 papers.

0numbers the graph read from it
0cells of the map it votes in
70citing papers in PubMed
9.1field-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

70 citing papers in PubMed, 112 citations in OpenAlex.

  1. Octopamine instructs head direction plasticity.bioRxiv : the preprint server for biology · 2025
    Article
  2. Article
  3. Review
  4. Review
  5. Article
  6. Integrins Bidirectionally Regulate the Efficacy of Inhibitory Synaptic Transmission and Control GABAergic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2022
    Article
  7. Article
  8. Review
  9. Article
  10. Article
  11. Impairment of Synaptic Plasticity by Cannabis, ΔCold Spring Harbor perspectives in medicine · 2021
    Review
  12. The endocannabinoid system in the amygdala and modulation of fear.Progress in neuro-psychopharmacology & biological psychiatry · 2021
    Review
  13. Multiple cannabinoid signaling cascades powerfully suppress recurrent excitation in the hippocampus.Proceedings of the National Academy of Sciences of the United States of America · 2021
    Article
  14. Review
  15. Article
  16. CBeLife · 2020
    Article
  17. Heterosynaptic GABAThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2019
    Article
  18. Review
  19. Article
  20. Synaptic plasticity mechanisms common to learning and alcohol use disorder.Learning & memory (Cold Spring Harbor, N.Y.) · 2018
    Review

10 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

3 authors at 1 institution in 1 country.

Boris D HeifetsDominick P Purpura Department of Neuroscience, Albert Einstein College of Medicine, Bronx, NY 10461, USA.
Vivien Chevaleyre
Pablo E Castillo
Albert Einstein College of Medicine · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Retrograde signaling by endocannabinoids (eCBs) mediates a widely expressed form of long-term depression at excitatory and inhibitory synapses (eCB-LTD), involving a reduction in neurotransmitter release. In the hippocampus, eCB-LTD occurs at interneuron (IN)-pyramidal cell (PC) synapses (I-LTD), and its induction requires a presynaptic reduction of cAMP/PKA signaling resulting from minutes of type 1 cannabinoid receptor (CB1R) activation. Although repetitive activity of glutamatergic synapses initiates the eCB mobilization required for I-LTD, it is unclear whether CB1R-containing GABAergic terminals are passive targets of eCBs or whether they actively contribute to induction. Here, we show that the minutes-long induction period for I-LTD may serve as a window to integrate associated spontaneous activity in the same IN receiving the retrograde eCB signal. Indeed, reducing spontaneous IN firing blocked I-LTD, which could be rescued with extra stimulation of inhibitory afferents. Moreover, cell pair recordings showed that a single IN expressed LTD onto a PC only if it was active during eCB signaling. Several methods of disrupting presynaptic Ca(2+) dynamics all blocked I-LTD, strongly suggesting that IN spikes regulate I-LTD by raising Ca(2+) at the nerve terminal. Finally, inhibiting the Ca(2+)-activated phosphatase, calcineurin, fully blocked I-LTD, but blocking another phosphatase did not. Our findings support a model where both CB1R signaling and IN activity shift the balance of kinase and phosphatase activity in the presynaptic terminal to induce I-LTD.

Indexed as

EndocannabinoidsAnimalsCalcineurinCalcineurin InhibitorsCalcium SignalingCannabinoid Receptor ModulatorsElectric StimulationElectrophysiologyHippocampusInterneuronsIn Vitro TechniquesLong-Term Synaptic DepressionNeuronal PlasticityPatch-Clamp TechniquesPyramidal CellsRatsCalcineurinCalcineurin InhibitorsCannabinoid Receptor ModulatorsEndocannabinoidsReceptor, Cannabinoid, CB1Tetrodotoxin

Identifiers

PMID18632563
PMCPMC2481322
OpenAlexW2040301525

What OpenQuestion holds

Textmetadata
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.