The Role of Caenorhabditis elegans Glutamate Transporters in a Model of Selenium-Induced Neurodegeneration
PublisherThe University of Arizona.
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AbstractSelenium is an essential micronutrient in low doses. However, high dose exposures to selenium induce cell loss, neuronal damage and other symptoms found in neurodegenerative diseases including Amyotrophic lateral sclerosis, Huntington’s, Parkinson’s, and Alzheimer’s diseases. In Caenorhabditis elegans (C. elegans), high dose selenium induces neurotoxicity that leads to a progressive movement impairment and death. Glutamate transporters (GLT) function in the synaptic cleft to remove excess glutamate and prevent excitotoxicity. Excitotoxicity has been shown to lead to neurodegeneration that has been found in previous studies to be related to neurological diseases. In C. elegans, there are six glutamate transporter genes, glt-1, -3, -4, -5, -6, and -7. Here we find that GLT-3 is more sensitive to the selenium-induced neurological effects. We also provide evidence that ceftriaxone increases the percentage of normal movement observed in selenium exposed animals, and that the glutamate transporters, GLT-4, GLT-5, and GLT-7 are necessary for ceftriaxone to function in C. elegans. Our findings provide additional insight of into the mechanisms of selenium-induced toxicity in C. elegans and support its use as a model for clarifying the mechanisms of neurological diseases. The experiment also sheds light on to the specific mechanisms by which ceftriaxone benefits movement in C. elegans.
Degree ProgramHonors College
Molecular and Cellular Biology