Status epilepticus is characterized by either a continuous seizure lasting for at least one hour or a series of intermittent seizures without restoration or normal EEG or behavioural patterns between successive seizures. Following status epilepticus, nerve cell loss and glyosis are found primarily in well localized sites of the limbic system, such as the hippocampal formation3, 6, s. The correlation between sustained epileptic seizures and the latter nerve cell loss is poorly understood. In order to examine this question, a technique would be needed to readily reproduce focal status epilepticus. Here we report that intra-amygdaloid application of kainic acid (KA), a potent analogue of glutamate 9, rapidly induces repetitive secondarily generalized convulsive seizures which culminate to fatal status epilepticus unless an anti-epileptic agent is administered. A preliminary report of this work was presented elsewhere 1. KA (0.4-1.6# g dissolved in 0.1-0.4# 1 phosphate buffer) was unilaterally injected into various amygdaloid nuclei of unanaesthetized and non-paralyzed male Wistar rats (n= 20). The injection was made via a delivery cannula (0.2 mm, id) which was inserted into a previously chronically implanted guide cannula (0.3 mm, id). In 8 rats conventional electrodes were also chronically implanted to allow simultaneous recording of the cortical and contralateral amygdaloid EEG. Following the injection, the behavioural and electrographic activity was examined for 2-6 h. Large doses of diazepam (valium, Roche, 20 mg/kg, ip) were usually given at the end of behavioural examination to prevent the death of the rat due to status epilepticus. One week later, the animals were anaesthetized, intracardially perfused with a 10% formalin solution and conventional histological procedures were then performed. Local application of KA induced typical focal amygdaloid seizures. As shown in Fig. 1, 6 min after KA application, epileptiform activity was apparent in the cortical record (A); this activity propagated to the contralateral amygdala 4 rain later (B). The first seizure was observed less than 12 min after KA application. The electrographic and motor characteristics were similar to those observed following electrical stimulation of the amygdala 4. In the order of appearance, we noted masticatory movements, myoclonia of the facial muscles, rearing on hindlimbs, paw tremor and falling. Abundant salivation was often also present. Seizures were observed at a frequency of