Ohara PT (2004) Exercise accelerates relapsing paralysis after recovery from spinal demyelination. Neuroscience 2004 Abstracts 419.6. Society for Neuroscience, San Diego, CA.
Summary: Exercise has been used to improve motor performance in humans and animals following spinal cord injury. The effects of exercise are generally positive but it is not known whether exercise is universally beneficial, particularly in rat models of spinal injury. We examined the spinal cord morphology and motor function recovery for 18 months in rats that had undergone lumbar spinal demyelination induced by CTB-saporin. Following the initial demyelination and paraplegia, motor function recovered and was stable for up to nine months after which there occurred a slow deterioration of function that occurred earlier and was more severe in rats that had been exercised on a treadmill. Rats given treadmill exercise starting three weeks after toxin injection had a mean motor deficit score of 3.0 (i.e. paraplegia) at perfusion while the non-treadmill treated rats had a mean score of 1.8 (SD 0.38, n = 6, p<0.05). Histological examination showed the same morphological changes occurred in both exercise and non-exercise treated animals including the loss of motoneurons, loss of spinal white matter and appearance of large spheroids of calcium in the ventral and dorsal horns and occasionally in the white matter. These findings suggest that, in addition to the acute effects of the toxin induced demyelination from which there is recovery of motor function, there are chronic irreversible effects of the toxin, or the initial demyelination, that cause a slow progressive degeneration of the spinal cord. This model might therefore be useful to study the long term effects of spinal insult of the type associated with conditions such as post-polio syndrome.
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