• Srikanth G Kanagal and Gillian D Muir.
• Department of Biomedical Sciences, Western College of Veterinary Medicine, 52 Campus Drive, University of Saskatchewan, Saskatoon, SK, Canada S7N 5B4. sri.kanagal@usask.ca
• Exp. Neurol. 2008 Dec 1;214(2):229-39.

AbstractThe purpose of this research was to investigate the compensatory role of undamaged spinal pathways after partial spinal injury in rats. We have previously shown that bilateral lesions of the dorsal funiculus (DF) at the cervical level caused changes in overground and skilled locomotion that affected the forelimbs more than the hindlimbs. The same lesions also caused fore-paw deficits during a skilled pellet retrieval task (Kanagal and Muir, 2007). In contrast, bilateral cervical lesions of the dorsolateral funiculus (DLF) caused alterations in overground and skilled locomotion that were most marked in the hindlimbs rather than the forelimbs, but also caused fore-paw deficits during skilled pellet retrieval (Muir et al., 2007). We hypothesized that the relative lack of forelimb deficits during locomotion after DLF lesions was due to compensatory input arising from intact pathways in the DF. We tested this hypothesis in the present study by performing bilateral DF lesions in animals in which both DLFs had been transected 6 weeks previously. These secondary DF lesions involved either only ascending sensory pathways (DLF+ASP group) in the DF, i.e. sparing the corticospinal tract (CST), or involved both the ASP and the CST (DLF+DF group). All animals were assessed during overground locomotion, while crossing a horizontal ladder and during a pellet retrieval task. During overground locomotion, both groups moved with slightly altered forces and timing in both forelimbs and hindlimbs. During both ladder crossing and reaching, secondary lesions to DF (with or without CST) exacerbated the deficits seen after initial DLF lesions and additionally caused changes in the manner in which the rats used their forelimbs during reaching. Nevertheless, the relative magnitude of the deficits indicates that DF pathways in rats likely do not compensate for loss of DLF pathways during the execution of locomotor tasks, though there is indirect evidence that DLF-lesioned rats might rely more on ascending sensory pathways in the DF during skilled forelimb movements. The plastic changes mediating recovery are therefore necessarily occurring in other regions of the CNS, and, importantly, need time to develop, because animals with DLF+DF lesions performed simultaneously displayed marked functional deficits and were unable to use their forelimbs for skilled locomotion or reaching.

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