title: Fate of the supraspinal collaterals of cord-projection neurons following upper spinal axonal injury.
abstract: In investigating the fate of the cord-projecting CNS neurons following spinal axonal injury, we have demonstrated that surviving rat rubrospinal neurons have altered electrical membrane properties so that their input/output relationship was increased. Further, we found that the synaptic inhibition they received from nearby reticular formation was also reduced following injury. Whether or not these property changes were functional was dependent on the output connections of injured neurons. In the current communication, we examined the supraspinal efferents of the injured neurons recognizing that normal neurons innervate not only spinal but also supraspinal targets. To this end we conducted anterograde tracing on the injured red nucleus 8 weeks following spinal lesion. Results showed that injured rubrospinal neurons still innervated the same supraspinal targets, targeted by normal neurons. We subsequently evaluated the relative intensity of the sustained supraspinal connectivity by examining, in detail, the cerebellar projection of rubrospinal neurons of similarly injured animals using retrograde tracing technique. Here our data revealed that the number, distribution and labeling intensity of rubrospinal neurons projecting to the cerebellum were unchanged following cord injury. In conclusion, although spinal cord injury deprive cord-projecting CNS neurons of their spinal targets, injured neurons survived with altered electrical membrane properties and intact supraspinal projections. The sustained supraspinal connections might allow injured cord-projecting CNS neurons to exert a different weight of influence on higher centers following spinal cord injury.
authors.affiliation: Department of Anatomy, College of Medicine, National Taiwan University, Taipei.
authors.forename: Y J
authors.initials: YJ
authors.lastname: Wang
authors.forename: H W
authors.initials: HW
authors.lastname: Ho
authors.forename: G F
authors.initials: GF
authors.lastname: Tseng
mesh_terms: D000818:Animals; D001369:Axons / Q000473:pathology* / Q000502:physiology*; D019771:Axotomy / Q000009:adverse effects; D001710:Biotin / Q000031:analogs & derivatives; D002529:Cerebellar Nuclei / Q000473:pathology / Q000503:physiopathology; D003911:Dextrans; D004525:Efferent Pathways / Q000473:pathology* / Q000503:physiopathology*; D005260:Female; D005456:Fluorescent Dyes; D009473:Neuronal Plasticity / Q000502:physiology; D051381:Rats; D017208:Rats, Wistar; D012012:Red Nucleus / Q000473:pathology* / Q000503:physiopathology*; D013116:Spinal Cord / Q000473:pathology* / Q000503:physiopathology*; D013119:Spinal Cord Injuries / Q000473:pathology* / Q000503:physiopathology*; D013997:Time Factors
chemical_list: D003911:Dextrans; D005456:Fluorescent Dyes; C076397:biotinylated dextran amine; D001710:Biotin