Preganglionic brachial plexus injuries fall into two categories according to the lesion site, root avulsion injury and root rupture injury. The latter type of injury involves part of the peripheral nervous system (PNS) component at the injured spinal cord surface. Previous investigators have used rhizotomy of experimental animals as a model for dorsal root rupture injury. However, the effect on the central nervous system (CNS)-PNS junction accompanied by the mechanical stress from traction force is hard to estimate in this model. The current study aimed to demonstrate temporal molecular alterations from the CNS-PNS junction to the ruptured dorsal root after traction injury by immunohistochemical procedures. At 28 days after dorsal rupture injury, GFAP-positive structures could be clearly identified showing rather straight lines from the centro-peripheral junction toward the peripheral stump in the ruptured dorsal root. Immunoelectron microscopy for GFAP verified GFAP IR within the astrocytic processes at the injured dorsal root at 28 days after dorsal rupture injury. Glial cell line-derived neurotrophic factor immunoreactivity (GDNF IR) was slightly upregulated within the Schwann cell bodies on the injured dorsal root at 24-48 h after rupture injury. However, GDNF IR had appeared showing a process-like profile on the ruptured dorsal root by 28 days, and it was closely related with GFAP-positive structures. In contrast, a small increase in GFAP IR was only detected on the proximal side on the rhizotomized dorsal root at 28 days after rhizotomy. A marked decrease in NF IR and S-100 IR was observed at the ruptured dorsal root from 7 days. On the other hand, laminin IR was strongly upregulated on the ruptured dorsal root from 48 h to 7 days, and was still evident at 28 days. We therefore conclude that the astrocytes show a unique ability to extend their processes toward the stump. This ability may provide a new medium for the study of axonal regeneration in future clinical experiments.
All Science Journal Classification (ASJC) codes
- Molecular Biology
- Clinical Neurology
- Developmental Biology