The omega-3 polyunsaturated acids (n-3 PUFA) show great promise as a therapy for epileptic seizures. There has been considerable confusion, however, in the animal data related to the n-3 PUFAs’ anticonvulsant effects. Our own recent work has clarified this confusion, and led to a simple, reproducible animal preparation in which to study the n-3 PUFAs’ mechanism(s) of action. We first attempted to replicate the studies of Yehuda et al. (1994), who had reported dramatic seizure suppression after 21 days of 40 mg/kg injections of the “SR 3” formula i.p in rats. In our replication, we found no effect at all at this dose (Taha et al., 2006). We therefore tested the higher dose of 200 mg/kg of the SR-3 mixture. At 200 mg/kg, we found a significant increase in PTZ seizure latency, although no change in severity (Taha et al., 2009). We subsequently tried acute administration of a single dose in rats, switching from SR 3 to docosahexaenoic acid (DHA). Injecting subcutaneously (s.c.), we found a significant elevation in PTZ-seizure latency following after a single injection (Taha et al., 2010). Our dose–response curves in this study, however, were “inverted U” shaped. In parallel studies, we tested dietary (p.o.) administration. Working in rats with chronically implanted electrodes, we found that dietary PUFAs elevated thresholds in both the cortex and the amygdala of rats. These effects, however, took several months to occur (Taha et al., in preparation). To simplify the kinetics, we have moved to intravenous (i.v.) injections of DHA (tail vein in rats). Our i.v. experiments have now shown anticonvulsant effects 5 min after injection and plasma concentrations that rise rapidly, plateau at 5 min, and drop to baseline a minute after infusion (Trepanier et al., in preparation). We have therefore finally evolved a preparation in which anticonvulsant effects and plasma concentrations parallel the known kinetics of DHA. This preparation will now allow a meaningful study of DHA’s mechanisms of anticonvulsant action.