Evidence map›Paper›PMID 19494194›Full record

ArticleJournal of neurophysiology2009

Cannabinoid CB1 receptor-dependent long-term depression in autaptic excitatory neurons.

Ryan Kellogg, Ken Mackie, Alex Straiker

Abstract read
In one paragraph

Article in Journal of neurophysiology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.

0numbers the graph read from it
0cells of the map it votes in
33citing papers in PubMed
3.8field-weighted citation impact, top 8% 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

33 citing papers in PubMed, 47 citations in OpenAlex.

  1. Review
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Restoring glutamate homeostasis in the nucleus accumbens via endocannabinoid-mimetic drug prevents relapse to cocaine seeking behavior in rats.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2021
    Article
  9. Review
  10. Article
  11. Crosstalk between the MCellular signalling · 2020
    Review
  12. Review
  13. Autaptic Cultures: Methods and Applications.Frontiers in synaptic neuroscience · 2020
    Article
  14. Structural Insights into CB1 Receptor Biased Signaling.International journal of molecular sciences · 2019
    Review
  15. Article
  16. Cannabinoid CBCannabis and cannabinoid research · 2017
    Review
  17. Article
  18. Article
  19. Review
  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

3 authors at 1 institution in 1 country.

Ryan KelloggDepartment of Anesthesiology, University of Washington, Seattle, Washington, USA.
Ken Mackie
Alex Straiker
University of Washington · US

Funding

Neuronal cannabinoidsR01DA011322 · NIDA · UNIVERSITY OF WASHINGTON · PI MACKIE, KENNETH · 1998 to 2014
$3.4M
Cannabinoid Modulation of Cell FunctionK05DA021696 · NIDA · TRUSTEES OF INDIANA UNIVERSITY · PI MACKIE, KENNETH · 2007 to 2017
$1.3M
NIDA NIH HHS DA-021696NIDA NIH HHS DA-11322NIDA NIH HHS K05 DA021696NIDA NIH HHS R01 DA011322
6 · The paper itself

Abstract

Long-term depression (LTD) of synaptic signaling-lasting from tens of minutes to hours or longer-is a widespread form of synaptic plasticity in the brain. Neurons express diverse forms of LTD, including autaptic LTD (autLTD) observed in cultured hippocampal neurons, the mechanism of which remains unknown. We have recently reported that autaptic neurons express both endocannabinoid-mediated depolarization-induced suppression of excitation (DSE) and metabotropic suppression of excitation (MSE). We now report that activating cannabinoid CB(1) receptors is necessary for the induction of autLTD. Most surprisingly, CB(1) does not induce autLTD via the G(i/o) proteins typically activated by this receptor nor with G(s). Rather, the requirements of presynaptic phospholipase C and filled calcium stores suggest G(q). In autLTD, a 3- to 4-min activation of the receptor by the endocannabinoid 2-arachidonoyl glycerol leads to prolonged inhibition while leaving short-term inhibition (e.g., DSE) intact. autLTD requires activation of both metabo- and ionotropic glutamate receptors. autLTD also requires MEK/ERK activation. Under certain conditions, one or more DSE stimuli will elicit autLTD. It is becoming evident that cannabinoids mediate multiple forms of plasticity at a single synapse, stretching temporally from tens of seconds (DSE/MSE) to tens of minutes (autLTD) to hours (CB(1) desensitization). Our findings imply a remarkable flexibility for the cannabinoid signaling system whereby discrete mechanisms of CB(1) activation within a single neuron yield temporally and mechanistically distinct forms of plasticity.

Indexed as

Analysis of VarianceAnimalsCells, CulturedElectric StimulationExcitatory Postsynaptic PotentialsExtracellular Signal-Regulated MAP KinasesHippocampusLong-Term Synaptic DepressionMAP Kinase Kinase KinasesMiceMice, KnockoutNeuronsPatch-Clamp TechniquesReceptor, Cannabinoid, CB1Receptors, GlutamateSynapsesExtracellular Signal-Regulated MAP KinasesMAP Kinase Kinase KinasesReceptor, Cannabinoid, CB1Receptors, Glutamate

Identifiers

PMID19494194
PMCPMC2724344
OpenAlexW2002381191

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.