Intra-ischemic extracellular release of dopamine and glutamate is associated with striatal vulnerability to ischemia.
We have previously described a marked attenuation of postischemic striatal neuronal death by prior substantia nigra (SN) lesion, and have shown that lowering the brain temperature by only a few degrees during ischemia also confers a marked protective effect. The present study was carried out to evaluate whether the protective effect of these manipulations involves changes in extracellular release of striatal dopamine (DA) and glutamate (Glu) during ischemia. Four animal subgroups were investigated, including unilateral SN-lesioned rats whose intra-ischemic brain temperature was maintained at 36 degrees C, and non-lesioned animals whose brain temperature was not regulated, or was maintained at 33 or 36 degrees C during ischemia. Striatal extracellular sampling was performed by a microdialysis probe in rats subjected to 20 min of ischemia by 4-vessel occlusion. In rats whose intra-ischemic brain temperature was 36 degrees C, both DA and Glu increased significantly. In SN-lesioned rats no changes were found in extracellular levels of DA. However, significant increases in Glu were measured. In animals whose brain temperature was not regulated (the intra-ischemic brain temperature fell to 30 degrees C) or maintained at 33 degrees C there was a significant increase of DA release, but no changes were found in extracellular levels of Glu. These results, taken together with the neuropathological findings, suggest that release of both DA and Glu during ischemia is necessary for the development of postischemic striatal damage.
D000818:Animals; D003342:Corpus Striatum / Q000378:metabolism / Q000503:physiopathology*; D004298:Dopamine / Q000378:metabolism*; D005971:Glutamates / Q000378:metabolism*; D018698:Glutamic Acid; D002546:Ischemic Attack, Transient / Q000378:metabolism*; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D005971:Glutamates; D018698:Glutamic Acid; D004298:Dopamine