Alterations in glutamate uptake and in expression of glutamate transporters have been identified in ALS patients; however studies on human specimens are done using post mortem samples that are only representative of the very late stage of the disease, characterized by massive motor neuron degeneration and severe tissue compromise. Mutant wobbler mice and transgenic SOD1G93A mice are the most used animal models for human ALS, and are considered a useful tool for studying mechanisms of motor neuron death potentially relevant to human disease. In this study a specific method for isolation of highly enriched synaptosomal fraction was set up to allow the evaluation of glutamate uptake characteristics in the presynaptic compartment. Results indicated that presynaptic terminals were able to clear glutamate through a high-affinity mechanism likely mediated by GLT1, in the absence of glial contamination.
Identifer | oai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:497391 |
Date | January 2009 |
Creators | Fumagalli, Elena |
Publisher | Open University |
Source Sets | Ethos UK |
Detected Language | English |
Type | Electronic Thesis or Dissertation |
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