Goto Tetsuya, Oh Seog Bae, Takeda Mamoru, Shinoda Masamichi, Sato Tadasu, Gunjikake Kaori K, Iwata Koichi
Department of Oral Anatomy and Cell Biology, Graduate School of Medical and Dental Sciences, Kagoshima University, Kagoshima, 890-6544, Japan.
Department of Neurobiology and Physiology, School of Dentistry, Seoul National University, Seoul, South Korea.
J Physiol Sci. 2016 Sep;66(5):381-6. doi: 10.1007/s12576-016-0448-1. Epub 2016 Mar 29.
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.
外周组织炎症可改变躯体感觉通路的特性，导致行为超敏反应，并使对有害刺激（痛觉过敏）和通常无害刺激（异常性疼痛）引起的疼痛反应增加。这些痛觉超敏反应是由三叉神经节（TG）神经元兴奋性的改变引起的。这些变化改变了延髓尾侧三叉神经核中神经元的感觉信息处理。关于三叉神经神经元-神经元/神经元-卫星神经胶质细胞（SGCs）通讯的信息越来越多。神经节内通讯的激活在三叉神经病理性疼痛的产生和维持中起重要作用。因此，在本综述中，我们关注正常和病理条件下TG神经元和SGCs感觉功能及药理调节的最新发现，并讨论神经胶质-神经元相互作用中潜在的治疗靶点，以预防三叉神经神经性疼痛和炎性疼痛。
