Evidence map›Paper›PMID 19321773›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2009

Localization of the endocannabinoid-degrading enzyme fatty acid amide hydrolase in rat dorsal root ganglion cells and its regulation after peripheral nerve injury.

Isobel J Lever, Michelle Robinson, Mario Cibelli, Cleoper Paule, Peter Santha, Louis Yee, Stephen P Hunt, Benjamin F Cravatt, Maurice R Elphick, Istvan Nagy and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.

0numbers the graph read from it
0cells of the map it votes in
35citing papers in PubMed
7.2field-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

35 citing papers in PubMed, 60 citations in OpenAlex.

  1. Trial
  2. Mechanistic Insights into the Analgesic Action of Acetaminophen: Its Bioactive Metabolite Induces Peripheral Analgesia in Addition to Central Analgesia.Medical principles and practice : international journal of the Kuwait University, Health Science Centre · 2026
    Review
  3. Article
  4. The analgesic paracetamol metabolite AM404 acts peripherally to directly inhibit sodium channels.Proceedings of the National Academy of Sciences of the United States of America · 2025
    Article
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  15. Review
  16. Review
  17. Pain hypersensitivity mechanisms at a glance.Disease models & mechanisms · 2013
    Review
  18. Article
  19. Article
  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

11 authors at 8 institutions in 4 countries.

Isobel J LeverPain Research Group, Department of Anaesthetics, Pain Medicine and Intensive Care, Faculty of Medicine, Imperial College London, Chelsea and Westminster Hospital Campus, London SW10 9NH, UK.
Michelle Robinson
Mario Cibelli
Cleoper Paule
Peter Santha
Louis Yee
Stephen P Hunt
Benjamin F Cravatt
Maurice R Elphick
Istvan Nagy
Andrew S C Rice
Imperial College London · GBAnesthesiology and Surgical Oncology Research Group · USChelsea and Westminster Hospital · GBQueen Mary University of London · GBScripps Research Institute · USUCL Australia · AUUniversity College London · GBUniversity of Szeged · HU

Funding

Medical Research Council G0801381Wellcome Trust
6 · The paper itself

Abstract

Fatty acid amide hydrolase (FAAH) is a degradative enzyme for a group of endogenous signaling lipids that includes anandamide (AEA). AEA acts as an endocannabinoid and an endovanilloid by activating cannabinoid and vanilloid type 1 transient receptor potential (TRPV1) receptors, respectively, on dorsal root ganglion (DRG) sensory neurons. Inhibition of FAAH activity increases AEA concentrations in nervous tissue and reduces sensory hypersensitivity in animal pain models. Using immunohistochemistry, Western blotting, and reverse transcription-PCR, we demonstrate the location of the FAAH in adult rat DRG, sciatic nerve, and spinal cord. In naive rats, FAAH immunoreactivity localized to the soma of 32.7 +/- 0.8% of neurons in L4 and L5 DRG. These were small-sized (mean soma area, 395.96 +/- 5.6 mum(2)) and predominantly colabeled with peripherin and isolectin B4 markers of unmyelinated C-fiber neurons; 68% colabeled with antibodies to TRPV1 (marker of nociceptive DRG neurons), and <2% colabeled with NF200 (marker of large myelinated neurons). FAAH-IR was also present in small, NF200-negative cultured rat DRG neurons. Incubation of these cultures with the FAAH inhibitor URB597 increased AEA-evoked cobalt uptake in a capsazepine-sensitive manner. After sciatic nerve axotomy, there was a rightward shift in the cell-size distribution of FAAH-immunoreactive (IR) DRG neurons ipsilateral to injury: FAAH immunoreactivity was detected in larger-sized cells that colabeled with NF200. An ipsilateral versus contralateral increase in both the size and proportion of FAAH-IR DRG occurred after spinal nerve transection injury but not after chronic inflammation of the rat hindpaw 2 d after injection of complete Freund's adjuvant. This study reveals the location of FAAH in neural tissue involved in peripheral nociceptive transmission.

Indexed as

EndocannabinoidsAmidohydrolasesAnimalsCannabinoid Receptor ModulatorsFatty Acid Amide HydrolasesFreund's AdjuvantGanglia, SpinalImmunohistochemistryInflammationMalePainRatsRats, WistarReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSciatic NerveAmidohydrolasesCannabinoid Receptor ModulatorsEndocannabinoidsFatty Acid Amide HydrolasesFreund's AdjuvantRNA, Messenger

Identifiers

PMID19321773
PMCPMC6665026
OpenAlexW2000628725

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.