Mechanisms of ectopic orofacial pain following peripheral nerve injury.

有文献报道三叉神经第3分支损伤后可引起三叉神经第2分支区感觉异常。我们推测，异常感觉的诱发可能与三叉神经节内神经胶质细胞和卫星细胞的信号传导有关。切断下牙槽神经后，艾德-1阳性细胞不仅分布于ATF 3阳性神经元周围，而且分布于三叉神经节外。推测艾德-1阳性细胞的诱导可能是由TNFα等细胞因子介导的，但未检测到NF-κB的诱导。此外，为了研究是否能诱导三叉神经节第1、2分支神经元的激活，还对神经元细胞外信号相关激酶（ERK）的磷酸化进行了讨论。然而，切断下牙槽神经后，von Frey细丝对胡须垫的机械刺激并没有诱导三叉神经节神经元中磷酸化ERK。

It has been reported that the injury of the 3rd branch of trigeminal nerve induced abnormal sensations in the area of the 2nd branch of trigeminal nerve. We hypothesized that the induction of the abnormal sensations were involved in the intra-ganglionic signaling via glial cells and satellite cells in the trigeminal ganglion. After transection of the inferior alveolar nerve, ED-1 positive cells were detected in through out of the trigeminal ganglion, not only around the ATF3 positive neurons. The induction of ED-1 positive cells was speculated to be mediated by cytokines such as TNFα, however, the induction of NF-κB was not detected. Furthermore, in order to investigate whether the activation of neurons in the 1st or 2nd branch of trigeminal ganglion could be induced, the phosphorylation of extracellular signal-related kinase(ERK) of the neurons was discussed. However, after the transection of inferior alveolar nerve, mechanical stimulation to the whisker pad by von Frey filaments did not induce the phosphorylated ERK in the trigeminal ganglion neurons.