Evidence map›Paper›PMID 24571856›Full record

ReviewThe Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry2015

Endocannabinoids in synaptic plasticity and neuroprotection.

Jian-Yi Xu, Chu Chen

Open access · greenAbstract readReview
In one paragraph

Review in The Neuroscientist : a review journal bringing neurobiology, neurology and psychiatry, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 71 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
71citing papers in PubMed, 1 pooled it
10.4field-weighted citation impact, top 1% 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

71 citing papers in PubMed, 1 synthesis or guideline pooled it, 139 citations in OpenAlex.

  1. Pooled it
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  8. Role of the Endocannabinoid System in Fibromyalgia.Current issues in molecular biology · 2025
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11 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 2 institutions in 2 countries.

Jian-Yi XuCancerControl Alberta, Alberta Health Services, Calgary, Alberta, Canada.
Chu ChenNeuroscience Center of Excellence, School of Medicine, Louisiana State University Health Sciences Center, New Orleans, LA, USA jianyi.xu@albertahealthservices.ca chen502@gmail.com.
Alberta Health Services · CALouisiana State University Health Sciences Center New Orleans · US

Funding

Endocannabinoids in Neurodegenerative DiseasesR01NS076815 · NINDS · UNIVERSITY OF TEXAS HLTH SCIENCE CENTER · PI CHU CHEN · 2012 to 2026
$4.2M
Endocannabinoids in COX-2-Mediated Synaptic Modification and NeurotoxicityR01NS054886 · NINDS · LSU HEALTH SCIENCES CENTER · PI CHEN, CHU · 2007 to 2010
$1.1M
MAGL Inhibition in Prevention and Treatment of Alzheimer's DiseaseR21AG039669 · NIA · LSU HEALTH SCIENCES CENTER · PI CHEN, CHU · 2011 to 2012
$337k
NIA NIH HHS R21 AG039669NIA NIH HHS R21AG039669NINDS NIH HHS R01 NS054886NINDS NIH HHS R01NS054886NINDS NIH HHS R01 NS076815NINDS NIH HHS R01NS076815
6 · The paper itself

Abstract

Endocannabinoids (eCBs) are endogenous lipid mediators involved in a variety of physiological, pharmacological, and pathological processes. While activation of the eCB system primarily induces inhibitory effects on both GABAergic and glutamatergic synaptic transmission and plasticity through acting on presynaptically expressed CB1 receptors in the brain, accumulated information suggests that eCB signaling is also capable of facilitating or potentiating excitatory synaptic transmission in the hippocampus. Recent studies show that a long-lasting potentiation of excitatory synaptic transmission at Schaffer collateral (SC)-CA1 synapses is induced by spatiotemporally primed inputs, accompanying with a long-term depression of inhibitory synaptic transmission (I-LTD) in hippocampal CA1 pyramidal neurons. This input timing-dependent long-lasting synaptic potentiation at SC-CA1 synapses is mediated by 2-arachidonoylglycerol (2-AG) signaling triggered by activation of postsynaptic N-methyl-D-aspartate receptors, group I metabotropic glutamate receptors (mGluRs), and a concurrent rise in intracellular Ca(2+). Emerging evidence now also indicates that 2-AG is an important signaling mediator keeping brain homeostasis by exerting its anti-inflammatory and neuroprotective effects in response to harmful insults through CB1/2 receptor-dependent and/or -independent mechanisms. Activation of the nuclear receptor protein peroxisome proliferator-activated receptor-γ apparently is one of the important mechanisms in resolving neuroinflammation and protecting neurons produced by 2-AG signaling. Thus, the information summarized in this review suggests that the role of eCB signaling in maintaining integrity of brain function is greater than what we thought previously.

Indexed as

Neuronal PlasticityNeuroprotectionAnimalsBrainBrain DiseasesEndocannabinoidsHippocampusHumansPyramidal CellsSignal TransductionEndocannabinoidsAlzheimer’s diseasechronic traumatic encephalopathyinput timing–dependent plasticitylong-term depression of inhibitory synaptic transmissionmonoacylglycerol lipasePPARγ

Identifiers

PMID24571856
PMCPMC4143501
OpenAlexW1989336822

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.