Abstract The effect of cocaine and lidocaine on the expression of kindled seizures was studied in male Long-Evans rats. Animals were implanted with an electrode in either the olfactory bulb, prepyriform cortex, or basolateral amygdala and kindled by daily electrical stimulation. Each animal was then tested for the expression of kindled seizures following the intraperitoneal administration of saline, 20 mg/kg cocaine hydrochloride, or 20 mg/kg lidocaine hydrochloride. During testing the implantation site was stimulated every 60 sec at increasing current levels until an afterdischarge was elicited. Each animal was tested once under each drug at 96 hr intervals. The order of drug administration was counterbalanced across animals. Neither cocaine nor lidocaine had a significant effect on afterdischarge threshold. Both drugs significantly reduced the latency for clonus to occur following stimulation, a measure presumably related to the propagation of afterdischarges from the site of stimulation to other brain areas. In addition both cocaine and lidocaine significantly reduced the rated behavioral response to the stimulation due to a decrease in rearing and falling. Because they occurred with both cocaine and lidocaine, these effects appear to be of local anesthetic origin. In contrast, only cocaine significantly reduced afterdischarge duration, and only lidocaine significantly reduced clonus intensity. With the possible exception of clonus latency, these effects were present at all electrode sites studied. The results indicate that cocaine has pronounced effects on the expression of seizure activity in the olfactory forebrain, some of which are due to its local anesthetic action, and some not.