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Accession IconGSE11141

Effects of NgR overexpression on the developing and mature forebrain (backm-affy-mouse-433094)

Organism Icon Mus musculus
Sample Icon 20 Downloadable Samples
Technology Badge Icon Affymetrix Mouse Genome 430 2.0 Array (mouse4302)

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The lack of axonal growth after injury in the adult central nervous system (CNS) is partly due to the presence of growth-inhibitory molecules associated with myelin and the intrinsic growth-state of the injured neurons. To date, three inhibitors have been identified in myelin: Myelin- Associated Glycoprotein (MAG), Nogo A, and Oligodendrocyte-Myelin glycoprotein (OMgp). These three proteins all appear to be located in the periaxonal surface of the myelin membrane placing them in an optimal location to mediate axon-glial interaction. In addition, the three proteins have been shown to bind the same neuronal receptor, known as the Nogo-66 receptor (NgR). It has been hypothesized that inhibition of NgR may be a strategy to increase regeneration, plasticity and functional recovery of the lesioned central nervous system. Strong NgR mRNA expression is observed in the hippocampal pyramidal cell layers (CA1-3) and the granular layer of the dentate gyrus. It has been shown that animals exposed to entorhinal lesions show a biphasic regulation of NgR in the hippocampus, suggesting a tightly regulated mechanism mediated by this receptor. We have access to a transgenic model to over-express NgR in forebrain hippocampal neurons. Preliminary results have shown a phenotypic response in behavior and some molecular markers, as result of NgR overexpression. Knowledge of what genes are reacting in this novel transgenic model may provide insights into what pathways are affected by NgR to control synaptic plasticity in normal animals and during injury.
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