In two experiments, involvement of norepinephrine in the development of status epilepticus was determined. Rats, pretreated with intraventricular 6-hydroxydopamine to deplete brain norepinephrine or with the saline vehicle alone, were implanted with electrodes in both amygdalae. In the first experiment, one amygdala was kindled to stage 5 levels and then 2 weeks later was stimulated continuously for 60 min in an effort to produce status epilepticus (SE), while in the second experiment such SE stimulation was applied to one amygdala without prior kindling. Although depletion of norepinephrine significantly facilitated amygdala kindling in experiment 1, it had no clear effect on the probability of developing SE (generalized, partial, or nonconvulsive) or on the distribution of gross brain pathology following spontaneous recovery from partial and nonconvulsive SE in either experiment. The significance of these results compared to other SE models was discussed.