Transient changes in BDNF parallel plasticity observed in the IML following distal axon injury

The neurotrophic regulation of sympathetic preganglionic neurons located in the intermediolateral cell column (IML) is poorly understood. We previously reported transient changes in the adult IML following injury to the cervical sympathetic trunk (CST), the distal axons entering the superior cervical ganglion (SCG). At 1 week following CST transection, activated astrocytes and microglia and increased numbers of trkB immunoreactive (−ir) oligodendrocytes populated the IML at levels C8-T1. This glial plasticity was paralleled by a decrease in choline acetyltransferase (ChAT)-ir neurons. Though ChAT was lost, neurons were present and expressed the injury marker activating transcription factor (ATF)-3. At 3 weeks, glial activation was absent, ChAT-ir neurons showed recovery, and ATF-3-ir neurons declined to 13% of IML neurons. The number and appearance of ChAT-ir neurons were similar to controls at 10 weeks following injury. The changes in trkB suggested a role for the neurotrophin brain derived neurotrophic factor (BDNF) during this period of plasticity and provided the basis for the present study where we used western blot analysis to investigate BDNF levels in the spinal cord at 1 week, 3 weeks, and 10 weeks following CST transection. At 1 week following injury, when glial cells respond and ChAT is decreased, the 24 kDa isoform showed a significant decrease in all cases and the 37 kDa isoform was decreased in 4 of the 5 cases examined. At 21 days, when gliosis has subsided and ChAT expression is recovering, the 37 kDa form was significantly increased. BDNF returned to control values at 10 weeks following injury. The transient changes in BDNF may play a role in the IML neuroplasticity observed following injury. The BDNF protein in the cord is likely produced locally since the transected axons do not reinnervate the SCG by 10 weeks and could not derive BDNF from their SCG target.