| Abstract No.: | C-F3175 |
| Country: | Canada |
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| Title: | LIVE IMAGING OF NEURONAL DAMAGE : A GAP43-GFP-LUC MOUSE MODEL |
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| Authors/Affiliations: | 1 Mathieu Gravel*; 1 Yuan Cheng Weng; 1 Jasna Kriz;
1 Centre de recherche du CHUQ, Department of Anatomy and Physiology, Québec, QC, Canada
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| Content: | Few techniques are currently available to follow the neuronal regeneration processes. In recent years, imaging strategies based on luminescent enzymes have been developed to study biological processes as they occur in living animals. The enzymatic reaction between luciferase and its substrate luciferin produce light, which can be detected by a high sensitivity CCD camera on the XENOGEN IVIS 200 Imaging System. To study neuronal regeneration from live animals, we generated transgenic mice carrying reporter genes luc and gfp under the transcriptional control of the growth associated protein 43 (GAP43) neuron specific promoter. GAP43 is almost exclusively neuronal and its expression occurs during development and axon regeneration. GAP43 is strongly expressed during nervous system development at embryonic and newborns stages and is thought to be involved in axonal outgrowth. The gene is then normally silent in adult nervous system. However, GAP43 can be strongly re-expressed after nerve and brain injuries. It has also been reported that GAP43 expression is significantly increased in the spinal cord of amyotrophic lateral sclerosis (ALS) patients. The GAP43-GFP-luc transgenic mice generated have first been analyzed in the context of acute nerve injury. Cerebral ischemia, induced by middle cerebral artery occlusion, and sciatic nerves lesions, induced by complete nerve cut or partial freeze-crushed nerve, both cause an induction of photon emissions. As expected, preliminary results obtained by immunohistochemistry show a co-localization of the transgenic GFP with NeuN (Neuronal specific marker) but not with neither GFAP (astrocytes specific) nor Iba1 (microglias/macrophages specific) suggesting that the transgene expression is neuronal specific. This mouse model will represent a unique tool for in-vivo studies of acute neuronal damage and chronic neurodegenerative disorders.
This study is supported by the CIHR and QTRN
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