Depletion of catecholamines (CAs) with intraventricular 6-hydroxydopamine (6-OHDA) has been repeatedly demonstrated to exert a profound facilatory influence on the rate of amygdala kindling in the rat. Since the depletion of noradrenaline (NE) effected by this neurotoxin is thought to mediate this acceleration in seizure development, it was hypothesized that acute administration of intraventricular NE prior to kindling stimulations would reverse this effect.
Male Wistar rats were pretreated with either intraventricular 6-OHDA or with the vehicle solution alone (VEH) and implanted with amygdala electrodes bilaterally. Following a minimum recovery period of three weeks, kindling was begun. Prior to each kindling stimulation, 6-OHDA and VEH animals received intraventricular infusions of either NE or the saline-ascorbic vehicle (ASC).
Pretreatment with 6-OHDA was once again found to facilitate the rate of kindling but, contrary to prediction, exogenous NE failed to reverse this effect. NE did however appear to retard kindling in VEH pretreated animals. These results are interpreted as evidence that the well-established seizure suppressive influence of NE is mediated presynaptically, presumably by the inhibitory α2 receptor.