In-vivo imaging of contusion spinal cord injury: the role of calcium signalling in axon sparing
Funded in: 2012, 2013, 2014
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The initial trauma due to spinal cord injury, results in a “primary”, direct, immediate and mostly mechanical destructive effect on the neurons. A secondary, indirect, long lasting and mostly neurobiochemically operated effect will damage additional neurons that were spared during the first impact. During these two processes, neurons that are damaged will degenerate over a delayed time course and will finally result in a corresponding loss of function. The degree of neuronal (axonal) survival will have a great impact on the quality of life after injury, the higher the number of neurons damaged, the higher the chances of functional loss.
This project aims at observing in vivo the axonal response after an experimental spinal cord injury. By spanning this observation over several hours or even days, it will be possible to map the fate of large numbers of axons during the acute injury.
From traumatic brain injury studies there is strong evidence for a role of calcium as a central regulator of axonal breakdown. Therefore a particular emphasis will be placed on monitoring this crucial ion and its triggered consequences, the project will focus on the role of calcium signalling and down-stream subcellular changes in the axons following a spinal cord injury.
Understanding the detailed calcium signalling mechanisms in single axons can answer fundamental questions about delayed axon damage following contusion. Such insight has the potential to help develop new treatment approaches to protect axons that survive the initial impact and that could increase in the end the quality of life of numerous patients.