Lack of axonal sprouting of spared propriospinal fibers caudal to spinal contusion injury is attributed to chronic axonopathy.
We have previously shown that a small percentage of long descending propriospinal tract (LDPT) axons are spared, whereas few short thoracic propriospinal (TPS) fibers survive 2 weeks following severe (50 mm weight drop) low thoracic spinal cord contusion injury (SCI). Here, we extended those findings to a moderate (25 mm weight drop) T9 SCI and assessed the effects of this lesion severity on propriospinal tract fibers at different time periods after injury. We anterogradely labeled fibers with fluororuby (FR) or WGA-HRP to determine their location and number 2, 4, 6, and 16 weeks post-SCI. Findings were compared with non-injured controls. At chronic time points, surviving FR-labeled LDPT fibers rostral to the injury remained as reactive endings or as putative regenerative sprouts. Caudal to the injury, spared LDPT fibers ran along a rim of lateral and ventral white matter, and ended as small abnormal-appearing putative terminal boutons or reactive endings within the intermediate gray matter of lumbosacral cord, with little axonal arborization and no evidence of injury-induced sprouting. One striking difference in the WGA-HRP experimental operates was the increased density of labeling of spared axons within the white matter caudal to the injury compared to controls. This labeling pattern was reminiscent of the labeling found after axotomy in studies by others, and raises a question as to contusion injury-induced impaired axonal transport. We hypothesize that axonal sprouting of axons after partial spinal cord injury seen in previous investigations was not found in the present investigation because of the additional pathological effects of contusion injury, similar to what is observed after traumatic brain injury.
Steencken
Amanda Conta
AC
Neuroscience Program, SUNY Upstate Medical University , Syracuse, New York, USA.
Siebert
Justin R
JR
Stelzner
Dennis J
DJ
D000818:Animals; D002908:Chronic Disease; D003911:Dextrans; D004195:Disease Models, Animal; D005260:Female; D020439:Growth Cones / Q000502:physiology* / Q000648:ultrastructure; D009413:Nerve Fibers, Myelinated / Q000473:pathology / Q000502:physiology; D009416:Nerve Regeneration / Q000502:physiology; D009434:Neural Pathways / Q000473:pathology / Q000503:physiopathology; D056347:Neuroanatomical Tract-Tracing Techniques; D009473:Neuronal Plasticity / Q000502:physiology*; D056325:Neuronal Tract-Tracers; D051381:Rats; D020318:Rats, Long-Evans; D020127:Recovery of Function / Q000502:physiology; D012235:Rhodamines; D013116:Spinal Cord / Q000473:pathology / Q000503:physiopathology*; D013119:Spinal Cord Injuries / Q000473:pathology / Q000503:physiopathology*; D014855:Wallerian Degeneration / Q000473:pathology / Q000503:physiopathology*; D018998:Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate
D003911:Dextrans; C067661:Fluoro-Ruby; D056325:Neuronal Tract-Tracers; D012235:Rhodamines; D018998:Wheat Germ Agglutinin-Horseradish Peroxidase Conjugate