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Growth-associated messenger ribonucleic acid expression in a model of successful central nervous system regeneration

University of British Columbia

Recent experiments examining the development and plasticity of the chick embryonic spinal cord have described its inherent ability to recover from injury suffered prior to embryonic day (E) 13. Severing the spinal cord on or before E12 resulted in complete anatomical and functional recovery, which defined the permissive period for repair. Transections performed on E13 or later resulted in paraplegia characteristic of the restrictive period for repair. Previous studies have described the expression of growth-associated proteins (GAPs) such as GAP 43 and a-tubulin which were expressed at high levels during axon extension, then down-regulated at the time of target contact. These proteins were also expressed during abortive attempts at regeneration, and characterized a genetic growth program which was recruited after injury. This study examined the neuronal response to injury as reflected by changes in growth-associated gene expression in the hindbrain measured using Northern blotting. Levels of mRNA for GAP 43 and total a-tubulin during normal development were found to peak at E10-12, the period of maximal outgrowth of brainstem-spinal projections. Complete spinal cord transections performed on Ell (successful repair) or E14 (unsuccessful repair) did not detectably alter total a-tubulin mRNA levels. GAP 43 mRNA levels were not detectably altered after Eli transection. In contrast, transection on E14 (unsuccessful repair) resulted in a maintained increase in GAP 43 mRNA levels at least until 7 days post-transection, the longest survival period studied. Northern blotting was likely not sensitive enough to detect the full complement of changes which occurred after injury. However, transaction during the restrictive period for repair resulted in a maintained increase in GAP43 mRNA expression. These data suggested that some brainstem-spinal projection neurons injured on E14 retained the inherent ability to re-express at least part of the axonal growth program, indicated by the appropriate re-expression of GAP 43 mRNA. This suggests that the presence of inhibitory influences (or the absence of facilitatory influences) after E13 may have prevented the re-growth of axons and the re-formation of appropriate synapses.

Thesis/Dissertation

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2008-09-05

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http://hdl.handle.net/2429/1672

Zoology

University of British Columbia

UBCV

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