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

Research output: Contribution to journalReview articlepeer-review

29 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)381-386
Number of pages6
JournalJournal of Physiological Sciences
Issue number5
Publication statusPublished - 2016 Sept 1


  • Allodynia
  • Hyperalgesia
  • Neuron
  • Pain
  • Satellite glial cell
  • Trigeminal ganglion


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