(en) While excitotoxicity and neuroinflammatory responses were clearly recognized as two essential mechanisms implicated in CNS diseases, it was only recently proposed that these two processes could be intrinsically linked. The aim of the present thesis was therefore to investigate the putative influence of neuroinflammation on the glutamatergic system. This study was performed in glial cells, as both astrocytes and microglia contribute to the regulation of synaptic transmission, the control of glutamate homeostasis and the inflammatory responses. Two main families of glutamatergic targets were studied because of their direct and/or indirect implications in glutamate control and in neuroinflammation: glutamate transporters (GLAST and GLT-1) and metabotropic glutamate receptors (mGluR3 and mGluR5). Inflammation-induced regulations of glutamatergic targets were investigated in vitro, but also in vivo in a neuropathic pain model. All together, the results of the present thesis highlight the crucial implication of neuroinflammation in CNS diseases through perturbations of glutamate homeostasis and of glial responses.
Affiliations
UCLouvainSSS/IONS/IONS - Institute of NeuroScience
Citations
APA
Chicago
FWB
Berger, J. (2011). Influence of neuroinflammation on the regulation of glutamate handling in astrocytes, link with neuropathies. https://hdl.handle.net/2078.5/152471