De Felipe C, Belmonte C
Instituto de Neurociencias, Universidad Miguel Hernandez, Ap. Correos 18, 03050 San Juan, Alicante, Spain.
Eur J Neurosci. 1999 Mar;11(3):899-906. doi: 10.1046/j.1460-9568.1999.00498.x.
The proto-oncogene c-Jun has been implicated in the control of neuronal responses to injury and in axonal growth during regenerative processes. We have investigated the expression of c-Jun during normal terminal remodelling in trigeminal ganglion neurons innervating the cornea and after acute injury of epithelial nerve terminals or parent axons. Remodelling and rearrangement, or damage limited to corneal epithelium endings, was not a trigger for activation of c-Jun expression. However, injury of parent axons in the stroma or in the orbital ciliary nerves induced c-Jun expression in 50% of the population of corneal neurons, which included all of the large myelinated and 20% of the small neuropeptide-containing corneal neurons. This suggests that c-Jun expression in trigeminal ganglion neurons is not associated with normal remodelling or regeneration of peripheral nerve terminals, and that it takes place only when parent axons are injured. A substantial number of damaged neurons do not express c-Jun, indicating that in primary sensory neurons, injury and regeneration may not always be coupled to the expression of this proto-oncogene.
原癌基因c-Jun已被证明与神经元对损伤的反应控制以及再生过程中的轴突生长有关。我们研究了支配角膜的三叉神经节神经元在正常终末重塑过程中以及上皮神经终末或母轴突急性损伤后c-Jun的表达情况。重塑和重排，或仅限于角膜上皮末梢的损伤，并非激活c-Jun表达的触发因素。然而，基质或眶睫状神经中母轴突的损伤在50%的角膜神经元群体中诱导了c-Jun表达，其中包括所有大的有髓鞘角膜神经元和20%的含小神经肽的角膜神经元。这表明三叉神经节神经元中c-Jun的表达与外周神经终末的正常重塑或再生无关，且仅在母轴突受损时发生。相当数量的受损神经元不表达c-Jun，这表明在初级感觉神经元中，损伤和再生可能并不总是与该原癌基因的表达相关联。
