In laboratory studies, counting the spinal motoneurons\nthat survived axonal injury is a major method to estimate\nthe severity and regenerative capacity of the injured motoneurons\nafter the axonal injury and rehabilitation surgery. However,\nthe typical motoneuron marker, the choline acetyltransferase\n(ChAT), could not be detected in the injured motoneurons\nwithin the first 3ââ?¬â??4 weeks postinjury. It is necessary to\nexplore the useful and reliable specific phenotypic markers to\nassess the fate of injured motoneurons in axonal injury. Here,\nwe used the fluorogold to retrograde trace the injured motoneurons\nin the spinal cord and studied the expression patterns\nof the alpha-motoneuron marker, the neuronal nuclei DNAbinding\nprotein (NeuN) and the peripheral nerve injury marker,\nthe activating transcriptional factor (ATF-3), and the oxidative\nstress marker, the neuronal nitric oxide synthase\n(nNOS) within the first 4 weeks of the root avulsion of the\nright brachial plexus (BPRA) in the adult male Sprague-\nDawley rats. Our results showed that ATF-3 was rapidly\ninduced and sustained to express only in the nuclei of the\nfluorogold-labeled injured motoneurons but none in the unaffected\nmotoneurons from the 24 h of the injury; meanwhile,\nthe NeuN almost disappeared in the avulsion-affected motoneurons\nwithin the first 4 weeks. The nNOS was not detected\nin the motoneurons until the second week of the injury. On the\nbasis of the present data, we suggest that ATF-3 labels\navulsion-injured motoneurons while NeuN and nNOS are\npoor markers within the first 4 weeks of BPRA.
Loading....