Electroencephalog., behavioral, and neuropathol. changes induced by infusion of quinolinic acid (Quin), an endogenous excitatory amino acid, into the dorsal hippocampus were investigated after 6-hydroxydopamine (6-OHDA) lesions of the dorsal noradrenergic bundle. 6-OHDA depletion of norepinephrine (NE) facilitated the expression of Quin-induced seizures in a low-dose group (20 nmol). However, the facilitatory effect was not observed in a high-dose group (120 nmol). A neuropathol. study indicated that central NE depletion did not influence the hippocampal cellular loss induced by intrahippocampal Quin infusion. The central NE system may play a role in the Quin-induced seizures.