Trigeminal ganglion neuronal activity and glial fibrillary acidic protein immunoreactivity after inferior alveolar nerve crush in the adult rat

Trigeminal ganglion neuronal activity and glial fibrillary acidic protein immunoreactivity after inferior alveolar nerve crush in the adult rat
复制标题

DOI:
10.1016/s0304-3959(97)00088-2
复制
发表时间:
1997-11-01
期刊:
影响因子:
7.4
通讯作者:
Byers, MR
Byers, MR
中科院分区:
医学1区
文献类型:
--
作者:
Chudler, EH;Anderson, LC;Byers, MR

文献摘要

被引文献

相似文献

三叉神经下颌部的神经损伤已被证明会引起卫星细胞反应,其延伸超出三叉神经节的下颌部进入上颌部和眼部。本研究的目的是确定是否有任何生理异常与这种分散的卫星细胞反应,我们研究了电生理和卫星细胞胶质细胞酸性蛋白免疫反应(GFAP-IR)的变化,发生在三叉神经节内的挤压伤后3,10和59天的下牙槽神经(IAN)。在IAN挤压后3天,对皮肤和口内结构的同侧刺激没有机械诱发反应(例如,下颌切牙、下唇和下颌牙龈)受IAN支配。然而,耳颞神经、下颌舌骨神经、舌神经和上颌神经的外周表象是完整的,并且对这些神经支配的组织的刺激没有检测到对机械刺激的异常反应。IAN挤压后10天,下颌神经元对IAN外周感受野的机械和电刺激作出反应,但与对照值相比,传导速度较慢,电阈值较高。这些异常的电生理反应特征在神经损伤后持续了59天。在IAN挤压后3,10和59天,3-4%的记录下颌神经元显示自发活动,从未观察到在没有神经损伤的大鼠。自发活动也从未观察到记录在三叉神经节的上颌或眼分裂的神经元。在三叉神经节的下颌部内,在神经损伤后3天观察到卫星细胞中的强烈GFAP-IR,平均131.7个神经元/切片,在10天观察到约50.3个神经元/切片。GFAP-IR也存在周围16.5和10.3神经元/节在上颌部的三叉神经在3和10天,分别。在IAN挤压后59天,在三叉神经的下颌部发现GFAP-IR卫星细胞约22.9个神经元/切片,但在三叉神经节的其他地方没有发现。与含有异常电生理反应的三叉神经节区域相比,被卫星细胞GFAP-IR包围的神经元的更广泛分布表明异常神经元信号传导可能不是被GFAP损伤反应包围的三叉神经节神经元的特征。然而,GFAP-LR在神经损伤后59天的持续性表明,卫星细胞GFAP参与了损伤神经元的长期恢复。(C)1997年国际疼痛研究协会。出版社:Elsevier Science B. V.
Nerve injury to the mandibular division of the trigeminal nerve has been shown to cause satellite cell reactions that extend beyond the mandibular division of the trigeminal ganglion into the maxillary and ophthalmic divisions. The goal of this study was to determine whether any physiological abnormalities correlated with this dispersal of satellite cell reaction, We investigated the electrophysiological and satellite cell glial fibrillary acidic protein immunoreactivity (GFAP-IR) changes that occur within the trigeminal ganglion 3, 10 and 59 days after a crush injury of the inferior alveolar nerve (IAN). At 3 days after IAN crush, there were no mechanically-evoked responses to ipsilateral stimulation of the skin and intraoral structures (e.g., mandibular incisor, lower lip and rostral mandibular gingiva) innervated by the IAN. However, the peripheral representations of the auriculotemporal, mylohyoid, lingual and maxillary nerve were intact and no abnormal responses to mechanical stimulation were detected to stimulation of tissue innervated by these nerves. By 10 days after the IAN crush, mandibular neurons responded to mechanical and electrical stimuli of the peripheral receptive field of the IAN, but with slower conduction velocities and higher electrical thresholds compared to control values. These abnormal electrophysiological response characteristics persisted 59 days following nerve injury. At 3, 10 and 59 days after IAN crush, 3-4% of the recorded mandibular neurons displayed spontaneous activity that was never observed in rats without nerve injury. Spontaneous activity was also never observed in neurons recorded in the maxillary or ophthalmic divisions of the trigeminal ganglion. Intense GFAP-IR in satellite cells was observed surrounding a mean of 131.7 neurons/section within the mandibular division of the trigeminal ganglion 3 days after nerve injury and around 50.3 neurons/section at 10 days. GFAP-IR was also present surrounding 16.5 and 10.3 neurons/section in the maxillary division of the trigeminal nerve at 3 and 10 days, respectively. At 59 days after IAN crush, GFAP-IR satellite cells were found around 22.9 neurons/section in the mandibular division of the trigeminal nerve, but were not found elsewhere in the trigeminal ganglion. The more extensive distribution of neurons encircled by satellite cell GFAP-IR compared to the trigeminal ganglion region containing abnormal electrophysiological responses demonstrates that abnormal neuronal signaling may not be characteristic of trigeminal ganglion neurons that are surrounded by GFAP injury reactions. However, the persistence of GFAP-LR 59 days after nerve injury suggests that satellite cell GFAP is involved in the long-term recovery of injured neurons. (C) 1997 International Association for the Study of Pain. Published by Elsevier Science B.V.