Figure 4.

Pharmacological profile of excitotoxic damage indicates that it is primarily mediated by kainate, not AMPA, receptors. In both acute and chronic experiments the concentration of applied kainate was 100 μM. Animals were killed 4–7 days after operation and diagrams drawn from Nissl stained longitudinal sections. The dashed areas represent the location of the lesion. GYKI53655 (100 μM), an AMPA-selective antagonist, did not greatly reduce the size of the lesion induced by kainate. Preferential activation of AMPA receptors, by glutamate applied in combination with cyclothiazide (both 100 μM), only caused small lesions. In all instances, kainate lesions were greatly reduced when the agonist was infused together with 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX; 30 μM). (Bar = 3 mm.)