Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Pharmacological blockade of fatty acid amide hydrolase (FAAH) by URB597 improves memory and changes the phenotype of hippocampal microglia despite ethanol exposure.

Biochemical pharmacology - 1 Nov 2018

Rivera Patricia, Fernández-Arjona María Del Mar, Silva-Peña Daniel, Blanco Eduardo, Vargas Antonio, López-Ávalos María Dolores, Grondona Jesús M, Serrano Antonia, Pavón Francisco Javier, Rodríguez de Fonseca Fernando, Suárez Juan

Abstract excerpt

Changes in endogenous cannabinoid homeostasis are associated with both ethanol-related neuroinflammation and memory decline. Extensive research is still required to unveil the role of endocannabinoid signaling activation on hippocampal microglial cells after ethanol exposure. Either microglial morphology, phenotype and recruitment may become notably altered after chronic alcohol-related neurodegeneration. Here,...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Arachidonic Acids
Share to Dentate Gyrus

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Endocannabinoids

Share to Glial Fibrillary Acidic Protein

Share to Memory, Short-Term

Share to Nitric Oxide Synthase Type II

Share to Polyunsaturated Alkamides

Share to Receptors, Chemokine

Source

Identifiers

PMID: 30098312
DOI: 10.1016/j.bcp.2018.08.005

Genes

FAAH
CCL2
CCR2
CCR4
CXCL12
TLR4

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Pharmacological blockade of fatty acid amide hydrolase (FAAH) by URB597 improves memory and changes the phenotype of hippocampal microglia despite ethanol exposure.PMID 30098312Read ↗

Ethanol induces neuroimmune dysregulation and soluble TREM2 generation in a human iPSC neuron, astrocyte, microglia triculture modelSemantic proximity Read ↗

Endocannabinoid Modulation of Microglial Phenotypes in NeuropathologySemantic proximity Read ↗

Increased expression of M1 and M2 phenotypic markers in isolated microglia after four-day binge alcohol exposure in male rats.Semantic proximity Read ↗

Sudden Cessation of Fluoxetine Before Alcohol Drinking Reinstatement Alters Microglial Morphology and TLR4/inflammatory Neuroadaptation in the Rat BrainSemantic proximity Read ↗

Deep proteome profiling reveals novel pathways associated with pro-inflammatory and alcohol-induced microglial activation phenotypes.Semantic proximity Read ↗

Microglial activation is not equivalent to neuroinflammation in alcohol-induced neurodegeneration: The importance of microglia phenotype.Semantic proximity Read ↗

Polygenic Risk for Alcohol Use Disorder Affects Cellular Responses to Ethanol Exposure in a Human Microglial Cell ModelSemantic proximity Read ↗

Microglia Phenotypes Following the Induction of Alcohol Dependence in Adolescent Rats.Semantic proximity Read ↗

Deep Proteomic Profiling of Human Stem Cell-Derived Microglia: Insights Into Inflammatory and Alcohol-Induced ReactivitySemantic proximity Read ↗

Cortical reactive microglia activate astrocytes, increasing neurodegeneration in human alcohol use disorderSemantic proximity Read ↗

Endocannabinoid signaling in brain diseases: Emerging relevance of glial cellsSemantic proximity Read ↗

Polygenic risk for alcohol use disorder affects cellular responses to ethanol exposure in a human microglial cell model.Semantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.