Abstract：
BACKGROUND: Following peripheral nerve damage, various non-neuronal cells are activated, triggering accumulation in the peripheral and central nervous systems, and communicate with neurons. Evidence suggest that neuronal and non-neuronal cell communication is a critical mechanism of neuropathic pain; however, its detailed mechanisms in contributing to neuropathic orofacial pain development remain unclear.
CONCLUSIONS: Neuronal and non-neuronal cell communication in the trigeminal ganglion (TG) is believed to cause neuronal hyperactivation following trigeminal nerve damage, resulting in neuropathic orofacial pain. Trigeminal nerve damage activates and accumulates non-neuronal cells, such as satellite cells and macrophages in the TG and microglia, astrocytes, and oligodendrocytes in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1-C2). These non-neuronal cells release various molecules, contributing to the hyperactivation of TG, Vc, and C1-C2 nociceptive neurons. These hyperactive nociceptive neurons release molecules that enhance non-neuronal cell activation. This neuron and non-neuronal cell crosstalk causes hyperactivation of nociceptive neurons in the TG, Vc, and C1-C2. Here, we addressed previous and recent data on the contribution of neuronal and non-neuronal cell communication and its involvement in neuropathic orofacial pain development.
CONCLUSIONS: Previous and recent data suggest that neuronal and non-neuronal cell communication in the TG, Vc, and C1-C2 is a key mechanism that causes neuropathic orofacial pain associated with trigeminal nerve damage.
CONCLUSIONS: Neuronal and non-neuronal cell communication in the trigeminal ganglion (TG) is believed to cause neuronal hyperactivation following trigeminal nerve damage, resulting in neuropathic orofacial pain. Trigeminal nerve damage activates and accumulates non-neuronal cells, such as satellite cells and macrophages in the TG and microglia, astrocytes, and oligodendrocytes in the trigeminal spinal subnucleus caudalis (Vc) and upper cervical spinal cord (C1-C2). These non-neuronal cells release various molecules, contributing to the hyperactivation of TG, Vc, and C1-C2 nociceptive neurons. These hyperactive nociceptive neurons release molecules that enhance non-neuronal cell activation. This neuron and non-neuronal cell crosstalk causes hyperactivation of nociceptive neurons in the TG, Vc, and C1-C2. Here, we addressed previous and recent data on the contribution of neuronal and non-neuronal cell communication and its involvement in neuropathic orofacial pain development.
CONCLUSIONS: Previous and recent data suggest that neuronal and non-neuronal cell communication in the TG, Vc, and C1-C2 is a key mechanism that causes neuropathic orofacial pain associated with trigeminal nerve damage.
摘要：
背景：周围神经损伤后，各种非神经元细胞被激活，触发周围和中枢神经系统的积累，并与神经元沟通。证据表明，神经元和非神经元细胞通讯是神经性疼痛的关键机制；然而，其导致神经性口面部疼痛发展的详细机制尚不清楚。
结论：三叉神经节（TG）中的神经元和非神经元细胞通讯被认为会导致三叉神经损伤后的神经元过度激活，导致神经性口面部疼痛。三叉神经损伤激活和积累非神经元细胞，如TG和小胶质细胞中的卫星细胞和巨噬细胞，星形胶质细胞,三叉神经脊髓尾核下（Vc）和上颈脊髓（C1-C2）中的少突胶质细胞。这些非神经元细胞释放各种分子，导致TG的过度激活，Vc,和C1-C2伤害性神经元。这些伤害性神经元释放增强非神经元细胞的分子。这种神经元和非神经元细胞串扰导致TG中伤害性神经元的过度激活，Vc,和C1-C2。这里,我们讨论了以前和最近的有关神经元和非神经元细胞通讯及其在神经性口面部疼痛发展中的作用的数据。
结论：以前和最近的数据表明，TG中的神经元和非神经元细胞通讯，Vc,C1-C2是引起与三叉神经损伤相关的神经性口面部疼痛的关键机制。
结论：三叉神经节（TG）中的神经元和非神经元细胞通讯被认为会导致三叉神经损伤后的神经元过度激活，导致神经性口面部疼痛。三叉神经损伤激活和积累非神经元细胞，如TG和小胶质细胞中的卫星细胞和巨噬细胞，星形胶质细胞,三叉神经脊髓尾核下（Vc）和上颈脊髓（C1-C2）中的少突胶质细胞。这些非神经元细胞释放各种分子，导致TG的过度激活，Vc,和C1-C2伤害性神经元。这些伤害性神经元释放增强非神经元细胞的分子。这种神经元和非神经元细胞串扰导致TG中伤害性神经元的过度激活，Vc,和C1-C2。这里,我们讨论了以前和最近的有关神经元和非神经元细胞通讯及其在神经性口面部疼痛发展中的作用的数据。
结论：以前和最近的数据表明，TG中的神经元和非神经元细胞通讯，Vc,C1-C2是引起与三叉神经损伤相关的神经性口面部疼痛的关键机制。
