Parkinson's disease (PD) is a neurodegenerative disorder, progressively affecting the dopaminergic neurons of the substantia nigra pars compacta (SNc) and thus leading to severe motor dysfunction. One of the mediators of neuronal death in PD is excitotoxicity, cell death as a result of increased extracellular glutamate (Glu) concentrations and subsequent overstimulation of ionotropic Glu receptors. Increased activity of the subthalamic nucleus has been observed in animal models for PD and may result in increased Glu release at the level of the output structures of the basal ganglia, i.e. substantia nigra pars reticulata (SNr) and entopeduncular nucleus. Since extracellular Glu concentrations are not only determined by the release but also by the re-uptake of Glu from the extracellular space, we studied the expression of the glial high-affinity Na+/K+-dependent Glu transporters, i.e. GLAST and GLT-1, in the SNr of 6-OHDA lesioned rats at different survival times post-lesion. For GLT-1 we clearly observed lower expression levels on the lesioned side compared to the intact side. At short survival times this is largely due to an increased expression on the intact side whereas at longer survival times this is due to a clear decrease in expression level on the lesioned side.
Original languageEnglish
Title of host publication7th Biannual meeting of the Belgian Society for Neuroscience
Publication statusPublished - 2007

    Research areas

  • Parkinson's disease, glutamate transport

ID: 1749574