Bilateral dorsal funicular lesions alter sensorimotor behaviour in rats

Spinal cord injury models often involve damage to the corticospinal tract (CST) because of the functional importance of this pathway in humans. In rats, the main component of the CST travels in the dorsal funiculus and cannot be damaged without concurrent damage to overlying sensory fibers. To distinguish deficits due to the loss of CST from those due to sensory fiber damage, we bilaterally axotomized ascending sensory fibers in dorsal columns without CST damage in one group of rats (ascending sensory pathways, ASP) and compared the results to a group with damage to ascending sensory fibers with CST damage (ASP+CST). We assessed the ability of rats to perform a skilled reaching task and to walk over a horizontal ladder. We also measured the forces exerted on the ground (ground reaction forces, GRF) and limb contact patterns produced during overground locomotion. After ASP lesions alone, endpoint measurements of reaching success and footslip errors on the ladder showed transitory impairments, although detailed analysis revealed persistent deficits in skilled forelimb movements. ASP+CST lesions caused persistent deficits in reaching success and ladder footslips throughout the 8-week post-surgical period. Measurement of GRFs and limb timing during overground locomotion revealed differences in both groups at 8 weeks post-surgery compared to pre-surgical values, but no differences between ASP and ASP+CST groups. These results emphasize the normal contribution of both ascending sensory axons and CST axons during skilled limb movements and support a role for ascending sensory information, but not descending CST input, during overground locomotion. These results also illustrate the value of using sensitive methods to reveal detailed behavioural changes after spinal injury.     

Task-dependent compensation after pyramidal tract and dorsolateral spinal lesions in rats

The purpose of this research was to investigate whether pathways in the dorsal part of the lateral spinal funiculus (DLF) can compensate for loss of corticospinal input (CST) to the spinal cord. The CST is known to control skilled limb movements in rats. The DLF contains several different pathways, including the rubrospinal tract (RST) which is also thought to influence limb movements. After lesions of either the corticospinal or the rubrospinal system, it is unclear how much of the remaining forelimb function is due to the presence of the alternate pathway. To begin to address this issue, the present study investigates the compensatory role of pathways in the DLF, including the rubrospinal tract, after bilateral lesions of the pyramidal tract (PT). We initially performed bilateral PT lesions in rats, which effectively removed the CST input to the spinal cord. We tested these rats during overground locomotion, skilled locomotion and skilled forelimb usage. After a 6 week recovery period, we then performed bilateral DLF lesions and compared the behavioural abilities of these rats to those of animals which underwent simultaneous PT and DLF lesions. If DLF pathways do compensate for PT lesions, then animals with PT lesions would rely more on DLF pathways than animals without PT lesions. Thus we hypothesized that animals with DLF lesions which were performed 6 weeks after PT lesions would exhibit more deficits on several behavioural tasks compared to animals which received PT and DLF lesions simultaneously. Our hypothesis was supported only for skilled pellet retrieval. Hence some DLF pathways, including the RST, were able to compensate for loss of CST input during skilled reaching but not during overground or skilled locomotion in PT-lesioned rats. These differential responses suggest that behavioural tasks vary in their reliance on specific pathways after injury, and, furthermore, that compensation for loss of specific connections can arise from numerous sources.     

Thoracic dorsal funicular lesions affect the bouton patterns on, and diameters of, layer VB pyramidal cell somata in rat hindlimb cortex

The effect of spinal dorsal funicular lesions (T 12) upon the frequency of boutons on, and diameters of the somata of pyramidal cells in layer VB of hindlimb cortex was studied. Adult rats sustained bilateral damage to either the dorsal column (DC, n = 10) alone or DC combined with the corticospinal tract (CS) (DC + CS, n = 34) and were utilized 1, 2, 3, 7, 14, 30, 45, 60, 90, or 120 days postoperatively (DPO). Neurons randomly sampled from 44 lesioned and 13 unoperated cases were analyzed for the number of silver-impregnated boutons (Rasmussen method) on the circumference of the soma as well as diameters of the soma, nucleus, and nucleolus. Analyses of variance comparing across lesioned and normal groups were significant for bouton counts on the soma (P less than 0.01), and diameters (long axis) of somata (P less than 0.01) and their nuclei (P less than 0.05). Both lesioned groups exhibited significant decreases from normal for these latter three parameters. With respect to survival time for the DC + CS-lesioned animals we noted the following: (1) Bouton counts on the soma significantly decreased below normal between 1 and 60 DPO; this decrease was most dramatic during the first three days postlesion. (2) Somal diameter (long axis) significantly decreased below normal between 2 and 120 DPO (except at 14 and 90 DPO). (3) Nuclear diameter (long axis) significantly decreased below normal only at 90 DPO. (4) Bouton counts on somata of neurons in layers VB and IV [Ganchrow and Bernstein, 1981] of hindlimb cortex correlated negatively and significantly across 120 postlesion days. The rapid shrinkage and reduced afferentation of layer VB somata during the first week following DC + CS lesions suggest initial, retrograde reactions to CS axotomy. Since bouton counts on layer VB somata were significantly less (P less than 0.05) in DC- than DC + CS-lesioned rats, it is hypothesized that CS axotomy regulated a set-point for increased afferentation which was maintained on the shrunken somata between 7 and 120 DPO.