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 Molecular mechanism of plasticity (AG Kreutz)

 Post-lesion plasticity after axon injury

Post-lesion plasticity after axon injury

Post-lesion plasticity after axon injury

Figure: Post-lesion plasticity after axon injury

To gain more insight into mechanisms of degeneration, regeneration and post-lesion plasticity we analyzed differential gene expression in the inner retina after optic nerve crush and developed a screening procedure for this purpose. We could demonstrate that one protein identified in this screen, MAP1b, is present in spontaneously regenerating axons. Interestingly, highly dynamic changes in the expression, phosphorylation and localization of cytoskeletal neurons were observed and it can be speculated that the regulation of these events will determine to a large degree the outcome of axon injury. Noteworthy , we could show that intraaxonal signal transduction via the cytoplasmic tyrosine kinase PYK2 is crucial for cell survival after axon injury and that PYK2 enhances NF-kappa B transcriptional activity. Moreover, we could demonstrate that inflammatory processes in the N. opticus are a crucial factor for the rearrangement of the retino-collicular projection after optic nerve crush.

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