Evidence map›Paper›PMID 22049424›Full record

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

Sustained firing of cartwheel cells in the dorsal cochlear nucleus evokes endocannabinoid release and retrograde suppression of parallel fiber synapses.

Miloslav Sedlacek, Philip W Tipton, Stephan D Brenowitz

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 12 papers.

0numbers the graph read from it
0cells of the map it votes in
12citing papers in PubMed
1.0field-weighted citation impact, top 31% 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

12 citing papers in PubMed, 26 citations in OpenAlex.

  1. Targeting the Limbic System: Insights into Its Involvement in Tinnitus.International journal of molecular sciences · 2023
    Review
  2. Review
  3. Article
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  10. Synaptic Zn2+ inhibits neurotransmitter release by promoting endocannabinoid synthesis.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013
    Article
  11. Article
  12. 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.

Miloslav SedlacekSection on Synaptic Transmission, National Institute on Deafness and Other Communication Disorders, National Institutes of Health, Bethesda, Maryland 20892, USA.
Philip W Tipton
Stephan D Brenowitz
National Institutes of Health · US

Funding

Synaptic plasticity and integration in neural circuits of the auditory systemZIADC000072 · NIDCD · NATIONAL INSTITUTE ON DEAFNESS AND OTHER COMMUNICATION DISORDERS · PI BRENOWITZ, STEPHAN · 2009 to 2014
$5.9M
Intramural NIH HHS ZIA DC000072
6 · The paper itself

Abstract

Neurons in many brain regions release endocannabinoids from their dendrites that act as retrograde signals to transiently suppress neurotransmitter release from presynaptic terminals. Little is known, however, about the physiological mechanisms of short-term endocannabinoid-mediated plasticity under physiological conditions. Here we investigate calcium-dependent endocannabinoid release from cartwheel cells (CWCs) of the mouse dorsal cochlear nucleus (DCN) in the auditory brainstem that provide feedforward inhibition onto DCN principal neurons. We report that sustained action potential firing by CWCs evokes endocannabinoid release in response to submicromolar elevation of dendritic calcium that transiently suppresses their parallel fiber (PF) inputs by >70%. Basal spontaneous CWC firing rates are insufficient to evoke tonic suppression of PF synapses. However, elevating CWC firing rates by stimulating PFs triggers the release of endocannabinoids and heterosynaptic suppression of PF inputs. Spike-evoked suppression by endocannabinoids selectively suppresses excitatory synapses, but glycinergic/GABAergic inputs onto CWCs are not affected. Our findings demonstrate a mechanism of transient plasticity mediated by endocannabinoids that heterosynaptically suppresses subsets of excitatory presynaptic inputs to CWCs that regulates feedforward inhibition of DCN principal neurons and may influence the output of the DCN.

Indexed as

EndocannabinoidsAction PotentialsAnesthetics, LocalAnimalsAnimals, NewbornBiophysicsCalciumCannabinoid Receptor ModulatorsCochlear NucleusDendritesElectric StimulationEnzyme InhibitorsEstrenesExcitatory Amino Acid AntagonistsFemaleGABA Antagonists1-(6-((3-methoxyestra-1,3,5(10)-trien-17-yl)amino)hexyl)-1H-pyrrole-2,5-dioneAM 251Anesthetics, LocalCalciumCannabinoid Receptor ModulatorsEndocannabinoidsEnzyme InhibitorsEstrenesExcitatory Amino Acid AntagonistsFG 9041GABA AntagonistsPicrotoxinPiperidinesPyrazolesPyrrolidinonesQuinoxalinesTetrodotoxin

Identifiers

PMID22049424
PMCPMC3234102
OpenAlexW2015460614

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.