Evidence map›Paper›PMID 19656360›Full record

ArticleMolecular pain2009

Adenovector GAD65 gene delivery into the rat trigeminal ganglion produces orofacial analgesia.

Jean-Philippe Vit, Peter T Ohara, Christopher Sundberg, Blanca Rubi, Pierre Maechler, Chunyan Liu, Mariana Puntel, Pedro Lowenstein, Maria Castro, Luc Jasmin

Open access · goldAbstract read
In one paragraph

Article in Molecular pain, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed
2.7field-weighted citation impact, top 10% 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

36 citing papers in PubMed, 54 citations in OpenAlex.

  1. Glial cells in neuropathic pain.Physiological reviews · 2026
    Review
  2. Article
  3. Article
  4. Article
  5. Article
  6. Pain Relief in a Trigeminal Neuralgia ModelFrontiers in cellular neuroscience · 2022
    Article
  7. Article
  8. α6GABANeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2021
    Article
  9. AAV-Mediated Combination Gene Therapy for Neuropathic Pain: GAD65, GDNF, and IL-10.Molecular therapy. Methods & clinical development · 2020
    Article
  10. Review
  11. Review
  12. Article
  13. Ganglionic GFAPJCI insight · 2017
    Article
  14. Article
  15. Article
  16. Review
  17. Article
  18. Article
  19. Engagement of the GABA to KCC2 signaling pathway contributes to the analgesic effects of A3AR agonists in neuropathic pain.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015
    Article
  20. Role of satellite glial cells in gastrointestinal pain.Frontiers in cellular neuroscience · 2015
    Review
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 3 institutions in 2 countries.

Jean-Philippe VitDepartment of Anatomy, University of California San Francisco, San Francisco, CA 94143, USA. Jeanpvit@gmail.com
Peter T Ohara
Christopher Sundberg
Blanca Rubi
Pierre Maechler
Chunyan Liu
Mariana Puntel
Pedro Lowenstein
Maria Castro
Luc Jasmin
Cedars-Sinai Medical Center · USUniversity of California, San Francisco · USUniversity of Geneva · CH

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundOur goal is to use gene therapy to alleviate pain by targeting glial cells. In an animal model of facial pain we tested the effect of transfecting the glutamic acid decarboxylase (GAD) gene into satellite glial cells (SGCs) of the trigeminal ganglion by using a serotype 5 adenovector with high tropisms for glial cells. We postulated that GABA produced from the expression of GAD would reduce pain behavior by acting on GABA receptors on neurons within the ganglion.

resultsInjection of adenoviral vectors (AdGAD65) directly into the trigeminal ganglion leads to sustained expression of the GAD65 isoform over the 4 weeks observation period. Immunohistochemical analysis showed that adenovirus-mediated GAD65 expression and GABA synthesis were mainly in SGCs. GABAA and GABAB receptors were both seen in sensory neurons, yet only GABAA receptors decorated the neuronal surface. GABA receptors were not found on SGCs. Six days after injection of AdGAD65 into the trigeminal ganglion, there was a statistically significant decrease of pain behavior in the orofacial formalin test, a model of inflammatory pain. Rats injected with control virus (AdGFP or AdLacZ) had no reduction in their pain behavior. AdGAD65-dependent analgesia was blocked by bicuculline, a selective GABAA receptor antagonist, but not by CGP46381, a selective GABAB receptor antagonist.

conclusionTransfection of glial cells in the trigeminal ganglion with the GAD gene blocks pain behavior by acting on GABAA receptors on neuronal perikarya.

Indexed as

Genetic TherapyAdenoviridaeAnalgesiaAnimalsChickensFacial PainGenetic VectorsGlutamate DecarboxylaseHumansMaleRatsRats, Sprague-DawleyTrigeminal GanglionGlutamate Decarboxylase

Identifiers

PMID19656360
PMCPMC2734545
OpenAlexW2129600547

What OpenQuestion holds

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LicenceCC BY
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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.