title: Recent advances in basic research on the trigeminal ganglion.
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.
authors.affiliation: Department 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.
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Goto
authors.affiliation: Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, South Korea.
authors.forename: Seog Bae
authors.initials: SB
authors.lastname: Oh
authors.affiliation: Department of Food and Life Sciences, School of Life and Environmental Sciences, Azabu University, Sagamihara, Japan.
authors.forename: Mamoru
authors.initials: M
authors.lastname: Takeda
authors.affiliation: Department of Physiology, School of Dentistry, Nihon University, Tokyo, Japan.
authors.forename: Masamichi
authors.initials: M
authors.lastname: Shinoda
authors.affiliation: Division of Oral and Craniofacial Anatomy, Graduate School of Dentistry, Tohoku University, Sendai, Japan.
authors.forename: Tadasu
authors.initials: T
authors.lastname: Sato
authors.affiliation: Department of Orthodontics, School of Dentistry, Kyushu Dental University, Kitakyushu, Japan.
authors.forename: Kaori K
authors.initials: KK
authors.lastname: Gunjikake
authors.affiliation: Department of Physiology, School of Dentistry, Nihon University, Tokyo, Japan.
authors.forename: Koichi
authors.initials: K
authors.lastname: Iwata
mesh_terms: D000818:Animals; D006930:Hyperalgesia / Q000503:physiopathology*; D009474:Neurons / Q000502:physiology*; D059225:Nociception / Q000502:physiology*; D010146:Pain / Q000503:physiopathology*; D012668:Trigeminal Ganglion / Q000502:physiology* / Q000503:physiopathology
keywords: Allodynia; Hyperalgesia; Neuron; Pain; Satellite glial cell; Trigeminal ganglion