SUMMARY1. Sodium di‐n‐propylacetate (DPA) treatment induced significant increases in brain contents of gamma‐aminobutyric acid (GABA), 5‐hydroxyindoleacetic acid (5‐HIAA) and homovanillic acid (HVA). Furthermore, the threshold for pentylenetetrazol (PTZ) clonic convulsions was also increased in response to DPA administration.2. Pretreatment with inhibitors of monoamine synthesis α‐methyl‐p‐tyrosine (AMPT) andp‐chlorophenylalanine (PCPA) did not alter the anticonvulsant activity of DPA, but when given alone, both AMPT and PCPA caused significant decreases in brain monoamine contents and PTZ threshold seizures.3. Experiments using probenecid suggest that the increases in 5‐HIAA and HVA seen after DPA treatment could have resulted from inhibition of their active transport out of the brain. These data indicate that the anticonvulsant action of DPA is not dependent on changes in monoamine met