Evidence map›Paper›PMID 25136293›Full record

ArticleFrontiers in cellular neuroscience2014

Novel endogenous N-acyl amides activate TRPV1-4 receptors, BV-2 microglia, and are regulated in brain in an acute model of inflammation.

Siham Raboune, Jordyn M Stuart, Emma Leishman, Sara M Takacs, Brandon Rhodes, Arjun Basnet, Evan Jameyfield, Douglas McHugh, Theodore Widlanski, Heather B Bradshaw

Open access · goldAbstract read
In one paragraph

Article in Frontiers in cellular neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 64 papers.

0numbers the graph read from it
0cells of the map it votes in
64citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

64 citing papers in PubMed, 116 citations in OpenAlex.

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4 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

10 authors at 1 institution in 1 country.

Siham RabouneDepartment of Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
Jordyn M StuartDepartment of Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
Emma LeishmanDepartment of Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
Sara M TakacsDepartment of Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
Brandon RhodesDepartment of Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
Arjun BasnetDepartment of Chemistry, Indiana University Bloomington IN, USA.
Evan JameyfieldDepartment of Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
Douglas McHughDepartment of Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
Theodore WidlanskiDepartment of Chemistry, Indiana University Bloomington IN, USA.
Heather B BradshawDepartment of Psychological and Brain Sciences, Indiana University Bloomington, IN, USA.
Indiana University Bloomington · US

Funding

Microglial activation by N-arachidonoyl glycineR21DA032150 · NIDA · TRUSTEES OF INDIANA UNIVERSITY · PI BRADSHAW, HEATHER BRYTE · 2011 to 2012
$424k
NIDA NIH HHS R21 DA032150
6 · The paper itself

Abstract

A family of endogenous lipids, structurally analogous to the endogenous cannabinoid, N-arachidonoyl ethanolamine (Anandamide), and called N-acyl amides have emerged as a family of biologically active compounds at TRP receptors. N-acyl amides are constructed from an acyl group and an amine via an amide bond. This same structure can be modified by changing either the fatty acid or the amide to form potentially hundreds of lipids. More than 70 N-acyl amides have been identified in nature. We have ongoing studies aimed at isolating and characterizing additional members of the family of N-acyl amides in both central and peripheral tissues in mammalian systems. Here, using a unique in-house library of over 70 N-acyl amides we tested the following three hypotheses: (1) Additional N-acyl amides will have activity at TRPV1-4, (2) Acute peripheral injury will drive changes in CNS levels of N-acyl amides, and (3) N-acyl amides will regulate calcium in CNS-derived microglia. Through these studies, we have identified 20 novel N-acyl amides that collectively activate (stimulating or inhibiting) TRPV1-4. Using lipid extraction and HPLC coupled to tandem mass spectrometry we showed that levels of at least 10 of these N-acyl amides that activate TRPVs are regulated in brain after intraplantar carrageenan injection. We then screened the BV2 microglial cell line for activity with this N-acyl amide library and found overlap with TRPV receptor activity as well as additional activators of calcium mobilization from these lipids. Together these data provide new insight into the family of N-acyl amides and their roles as signaling molecules at ion channels, in microglia, and in the brain in the context of inflammation.

Indexed as

endocannabinoidslipid signalingmicrogliaN-acyl amidesTRP receptors

Identifiers

PMID25136293
PMCPMC4118021
OpenAlexW2118998202

What OpenQuestion holds

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Registered trials

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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.