Annual Meeting of the Society for Neuroscience edition:31 location:San Diego, U.S.A. date:November 10-15, 2001
Previous microdialysis experiments revealed a role for glutamate (Glu) and aspartate (Asp) in cortical reorganization as induced by homonymous central retinal lesions. Asp and Glu concentrations were significantly lower in lesion-affected area 17 compared to non-affected visual cortex. To determine whether these differences were a consequence of a change in the removal of Glu and Asp from the synaptic cleft, we perfused the microdialysis probe with a potent and selective inhibitor of glutamate transporters, L-trans-pyrrolidine-3,4-dicarboxylic acid. This resulted in increased Asp (745%) and Glu (438%) concentrations in area 17 of control animals. In retinal lesion cats, Asp and Glu levels increased 924% and 714% in lesion-affected area 17 compared to 476% and 337% in non-affected visual cortex. Blocking the transporters induced almost equal Asp and Glu concentrations in both brain regions. Western blotting revealed higher concentrations for the glial glutamate transporters, GLAST and GLT-1, in lesion-affected area 17 compared to non-affected visual cortex. In conclusion, the altered cortical extracellular Glu and Asp concentrations following retinal lesions are, at least partially, a consequence of altered re-uptake from the synaptic cleft. This difference in re-uptake results from altered expression of the glial glutamate transporters and possibly also from a difference in activity of one or more of the high-affinity glutamate transporters.