Evidence map›Paper›PMID 27023716›Full record

ReviewThe journal of physiological sciences : JPS2016

Recent advances in basic research on the trigeminal ganglion.

Tetsuya Goto, Seog Bae Oh, Mamoru Takeda, Masamichi Shinoda, Tadasu Sato, Kaori K Gunjikake, Koichi Iwata

Open access · goldAbstract readReview
In one paragraph

Review in The journal of physiological sciences : JPS, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
3.5field-weighted citation impact, top 8% 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

21 citing papers in PubMed, 41 citations in OpenAlex.

  1. Article
  2. Review
  3. Review
  4. Review
  5. Review
  6. Article
  7. Pain Relief in a Trigeminal Neuralgia ModelFrontiers in cellular neuroscience · 2022
    Article
  8. Review
  9. Review
  10. The fifth cranial nerve in headaches.The journal of headache and pain · 2020
    Review
  11. Article
  12. Review
  13. Article
  14. Review
  15. Corneal pain and experimental model development.Progress in retinal and eye research · 2019
    Review
  16. Review
  17. Article
  18. Review
  19. TFOS DEWS II pain and sensation report.The ocular surface · 2017
    Review
  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

7 authors at 6 institutions in 2 countries.

Tetsuya GotoDepartment of Oral Anatomy and Cell Biology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, 890-6544, Japan. tgoto@dent.kagoshima-u.ac.jp.
Seog Bae OhDepartment of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, South Korea.
Mamoru TakedaDepartment of Food and Life Sciences, School of Life and Environmental Sciences, Azabu University, Sagamihara, Japan.
Masamichi ShinodaDepartment of Physiology, School of Dentistry, Nihon University, Tokyo, Japan.
Tadasu SatoDivision of Oral and Craniofacial Anatomy, Graduate School of Dentistry, Tohoku University, Sendai, Japan.
Kaori K GunjikakeDepartment of Orthodontics, School of Dentistry, Kyushu Dental University, Kitakyushu, Japan.
Koichi IwataDepartment of Physiology, School of Dentistry, Nihon University, Tokyo, Japan.
Nihon University · JPAzabu University · JPKagoshima University · JPKyushu Dental University · JPSeoul National University · KRTohoku University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Peripheral tissue inflammation can alter the properties of somatic sensory pathways, causing behavioral hypersensitivity and resulting in increased responses to pain caused by noxious stimulation (hyperalgesia) and normally innocuous stimulation (allodynia). These hypersensitivities for nociception are caused by changes in the excitability of trigeminal ganglion (TG) neurons. These changes alter sensory information processing in the neurons in the medullary trigeminal nucleus of caudalis. Increasing information is becoming available regarding trigeminal neuron-neuron/neuron-satellite glial cells (SGCs) communication. The activation of intraganglionic communication plays an important role in the creation and maintenance of trigeminal pathological pain. Therefore, in this review, we focus on the recent findings for sensory functions and pharmacological modulation of TG neurons and SGCs under normal and pathological conditions, and we discuss potential therapeutic targets in glia-neuronal interactions for the prevention of trigeminal neuropathic and inflammatory pain.

Indexed as

AnimalsHyperalgesiaNeuronsNociceptionPainTrigeminal GanglionAllodyniaHyperalgesiaNeuronPainSatellite glial cellTrigeminal ganglion

Identifiers

PMID27023716
PMCPMC10717556
OpenAlexW2324307632

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.