Anderson L C, von Bartheld C S, Byers M R
Department of Oral Biology, University of Washington, Seattle, Washington 98195, USA.
Exp Neurol. 1998 Apr;150(2):312-20. doi: 10.1006/exnr.1997.6769.
Following peripheral nerve injury, neuronal cell functions in sensory ganglia shift from normal maintenance and neurotransmission toward survival and regeneration. A rapid modulation of glial cell activity, which is related to changes in neuronal-support cell interaction, also occurs after nerve injury. Nerve growth factor (NGF) is required for the survival and maintenance of specific populations of sensory and sympathetic neurons, and changes in neuronal gene expression after axonal injury are due in part to a loss of NGF retrograde transport from the periphery to the cell body. A similar role for NGF in modulating support cell responses to peripheral nerve injury, however, has not been demonstrated. Using an autoimmune model, we assessed the effects of NGF depletion in adult rats on the injury-induced expression of glial fibrillary acid protein immunoreactivity (GFAP-IR) in the ipsilateral and contralateral trigeminal ganglia (TG). Unilateral inferior alveolar nerve crush resulted in a bilateral, NGF-dependent trigeminal satellite cell response. In control rats there was a widespread induction of GFAP-IR in the ipsilateral as well as the contralateral TG. In contrast, GFAP-IR was reduced to the mandibular division of the ipsilateral TG in NGF-depleted rats, and the contralateral up-regulation of GFAP-IR was entirely abolished. Bilateral sympathectomy failed to mimic the effects of autoimmunization. Our results provide evidence that NGF depletion inhibits injury-induced satellite cell responses, independent of its effects on sympathetic nerve function.
周围神经损伤后，感觉神经节中的神经元细胞功能从正常维持和神经传递转向存活和再生。神经损伤后也会迅速调节神经胶质细胞活性，这与神经元-支持细胞相互作用的变化有关。神经生长因子（NGF）是特定感觉神经元和交感神经元群体存活和维持所必需的，轴突损伤后神经元基因表达的变化部分归因于NGF从外周向细胞体的逆行运输丧失。然而，NGF在调节支持细胞对周围神经损伤反应中的类似作用尚未得到证实。我们使用自身免疫模型评估了成年大鼠中NGF耗竭对同侧和对侧三叉神经节（TG）中损伤诱导的胶质纤维酸性蛋白免疫反应性（GFAP-IR）表达的影响。单侧下牙槽神经挤压导致双侧NGF依赖性三叉神经卫星细胞反应。在对照大鼠中，同侧和对侧TG中均广泛诱导了GFAP-IR。相比之下，在NGF耗竭的大鼠中，GFAP-IR减少至同侧TG的下颌分支，并且对侧GFAP-IR的上调完全被消除。双侧交感神经切除术未能模拟自身免疫的效果。我们的结果提供了证据，表明NGF耗竭抑制损伤诱导的卫星细胞反应，与其对交感神经功能的影响无关。
