Weanling male rats were fed hydrogenated coconut oil to induce essential fatty acid (EFA) deficiency. After 15 weeks, the rats were divided into six groups. Five groups were fed graded amounts of purified linolenate (18:3 omega 3) with a constant amount of linoleate (18:2 omega 6) for six weeks. Fatty acid composition was determined in brain lipids. Increasing dietary 18:3 omega 3 resulted in a decrease in arachidonic acid (20:4 omega 6), docosatetraenoic acid (22:4 omega 6) and docosapentaenoic acid (22:5 omega 6), whereas 18:2 omega 6 and eicosatrienoic acid (20:3 omega 6) were increased both in total lipids and phospholipids. These results suggest that dietary 18:3 omega 3 exerts its inhibitory effect mainly on the desaturation of 20:3 omega 6 to 20:4 omega 6 in brain lipids. Linolenate was undetectable in brain lipids from any dietary treatments. The levels of eicosapentaenoic acid (20:5 omega 3) in groups receiving dietary 18:3 omega 3 were not different from that of the group receiving no 18:3 omega 3. These results indicate that, in the brain, 18:3 omega 3 is rapidly converted mainly to 22:6 omega 3 without being accumulated and imply that dietary 18:3 omega 3 can modulate the level of precursor of diene prostaglandins (PG) but not that of triene PG in the rat brain.