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An investigation into the potential for activity‐dependent regeneration of the rubrospinal tract after spinal cord injury
Author(s) -
Harvey Philip J.,
Grochmal Joey,
Tetzlaff Wolfram,
Gordon Tessa,
Bennett David J.
Publication year - 2005
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2005.04514.x
Subject(s) - stimulation , spinal cord , red nucleus , neuroscience , central nervous system , antidromic , biology , nucleus
We tested whether regeneration of transected rubrospinal tract (RST) axons is facilitated by a prolonged electrical stimulation of these axons. A peripheral nerve was grafted to the transected RST at the cervical level (C4/5) of adult rats, providing a permissive environment for regeneration of rubrospinal axons. Direct antidromic stimulation of the RST was applied immediately after grafting through a microwire inserted just rostral to the RST lesion, using a 1‐h 20‐Hz supramaximal stimulation protocol. Stimulation caused no direct damage to rubrospinal axons, and was sufficient to recruit the entire rubrospinal tract. In control animals that had a nerve graft and implanted microwire with no stimulation, there were 42.7 ± 10.2 rubrospinal neurons regenerated into the graft at 8 weeks, as assessed by retrograde labelling. In test animals that were stimulated there were 28.2 ± 7.4 backlabelled neurons, not significantly different from control, indicating that this stimulation did not improve the regenerative capacity of rubrospinal neurons. Furthermore, reverse‐transcriptase polymerase chain reaction and in situ hybridization for brain‐derived neurotrophic factor (BDNF) and/or growth‐associated protein‐43 (GAP‐43) expression in rubrospinal neurons revealed no significant difference between stimulated and unstimulated groups at 48 h after injury, with either 1 or 8 h of stimulation. In summary, direct stimulation of the injured RST axons for the periods tested does not increase expression of GAP‐43 and BDNF, and ultimately does not promote regeneration of these central nervous system axons.