口腔顔面の神経障害性疼痛発症に対する神経細胞‒非神経細胞機能連関の関与

Following trigeminal nerve injury, allodynia and hyperalgesia can occur in a wide area of the orofacial region innervated by the injured and uninjured nerves. Various non-neuronal cells, such as macrophages, T cells, and neurocytes, accumulate in the trigeminal ganglion as well as the injured sites. These non-neuronal cells release a variety of molecules, including cytokines, ATP, and neuropeptides, affecting the neuronal excitability of trigeminal ganglion neurons and causing the TG neurons to become hyperactive. Satellite cells are also activated following trigeminal nerve injury, and the activated satellite cells release a variety of molecules, enhancing TG neuronal activity. The barrage of action potentials generated in TG neurons is conveyed to the higher central nervous system, such as the trigeminal spinal subnucleus caudalis(Vc)and the upper cervical spinal cord(C1-C2), and the Vc and C1-C2 nociceptive neurons become hyperactive. Various non-neuronal cells, astrocytes, microglia, and oligodendrocytes are subsequently activated. In the Vc and C1-C2 regions, neurons and non-neuronal cells communicate with each other via a variety of molecules, such as cytokines, NO, neurotrophic factors, and neuropeptides. These mechanisms of neuron-non-neuronal cell communication in the TG and Vc and C1-C2 regions are thought to be key mechanisms underlying the development of orofacial neuropathic pain.