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Title: Behavioural consequences of demyelination and remyelination in the dorsal funiculus of the rat spinal cord
Author: Jeffrey, N. D.
Awarding Body: University of Cambridge
Current Institution: University of Cambridge
Date of Award: 1997
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This project aimed to investigate the behavioural effects of demyelination, spontaneous remyelination and transplant-mediated remyelination in the dorsal funiculus of the rat spinal cord. Neurological deficits were detected on a beam walking test after photochemical ablation of the dorsal funiculus of the rat lumbar spinal cord, suggesting the potential of this test for evaluation of demyelinating lesions. The severity of the locomotor deficits correlated with the extent of tissue destruction. When an intraspinal injection of ethidium bromide was used to induce a zone of demyelination in the dorsal funiculus of the cervical spinal cord there was impairment of locomotor efficiency during beam walking. The severity of locomotor impairment in this and most subsequent experiments was related to the size of the demyelinating lesion and the severity of axonal injury. Behavioural deficits resolved spontaneously so that recovery occurred by about 5 weeks post operatively. If remyelination was inhibited by exposure of the injected region to 40 Gray of x-irradiation behavioural recovery did not occur. In another group of rats, repeated injection of gliotoxin into a remyelinated ethidium bromide lesion caused recurrence of behavioural deficits. Injection of a mixed glial cell suspension into non-repairing (irradiated) ethidium bromide lesions initially did not produce superior behavioural recovery to that observed in control (non-transplanted) animals. However, transplantation into non-irradiated lesions did not prevent behavioural recovery. The study provides strong evidence that demyelination leads to loss of normal locomotor behaviour and that remyelination restores lost function. The failure to demonstrate conclusively that transplant-mediated remyelination restores function lost because of demyelination is probably the result of extensive axonal injury during lesioning and transplantation procedures.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available