The arachidonic acid (AA) metabolites prostaglandin D2 (PGD2), prostaglandin E2 (PGE2), prostaglandin F2 alpha (PGF2 alpha) and thromboxane B2 (TXB2) were measured in the dorsal hippocampus, amygdala/pyriform cortex and parietal cortex of the rat brain following the application of kainic acid (KA, s.c. 10 mg/kg). The first significant increases in the prostanoids were seen 10 min following the KA injection, at this time the first behavioral change 'staring' was observed. In the hippocampus the highest concentrations of the PGs were reached 30 min after the injection of the neurotoxin. At this time frequent wet dog shakes (WDS) and rare focal convulsions effecting head and extremities occurred. In the amygdala/pyriform cortex and parietal cortex the maximal prostanoid formation was seen after 120 min. At this time tonic clonic seizures were registered. In contrast to other seizure models, where PGD2 was the predominant prostanoid formed, PGF2 alpha was the major AA-metabolite found in KA-treated animals. From the time-course of the seizure-related behavior and the increased prostanoid synthesis we conclude that the initiation of the prostanoid synthesis was triggered by the increased neuronal activity rather than by cell damage.