The physiology and morphology of thoracic interneurons following spinal cord injury
The physiology and morphology of thoracic spinal neurones has previously been described. This thesis now examines plasticity with respect to this population of cells in the segment rostral to a partial spinal cord injury. Intracellular penetrations were made of ventral horn interneurones, one segment rostral to an ipsilateral spinal hemisection. This was done in conjunction with extracellular recordings of expiratory bulbospinal neurones in the medulla. Spike-triggered averaging was performed to reveal new connection to the interneurones from sprouting EBSNs. The yield however, was too low to draw any valid conclusions Intracellularly penetrated interneurones were iontophoretically labelled with neurobiotin. The axons and dendritic trees were completely reconstructed. No significant difference was found overall between the control and the lesion populations in terms of numbers of collateral branches from the first 3mm of axon, although this parameter was affected by distance of the soma from the lesion and survival time. Axon collaterals terminated in a significantly larger proportion of the ventral horn/intermediate zone than in controls. This effect was significantly affected by distance from the lesion and survival time and was most prominent in the intermediate zone. These observations are taken as being indicative of axonal sprouting, although alternative hypothesis are discussed. The dendritic trees of the interneurones showed unusual features indicative of sprouting. These included tangled structures, twisted dendrites, commissural dendrites, unusually thick proximal dendrites, a lack of normal dendritic tapering, right angle branching and an overall asymmetry of the dendritic tree. Distal branches of an interneurone labelled for the cytoskeletal dendritic protein, MAP2a/b lacked immuno-labelling for this protein. Overall, MAP 2a/b labelling was noted to be less dense on the lesion side compared to the non-lesioned side of the spinal cord. Thus new forms of plasticity have been demonstrated in uninjured interneurones in the injured spinal cord.