Arachidonic acid has been proposed as a diffusible second messenger in the CNS with a pathophysiological role in epilepsy and stroke and a physiological role in long-term potentiation. These actions are possibly due to the ability of arachidonic acid to enhance extraneuronal glutamate concentration. In this present study we have investigated the effect of flurbiprofen, a cyclo-oxygenase inhibitor, on both potassium- and veratridine-stimulated release of glutamate from rat cerebellar slices. Flurbiprofen (100–500 μ M) had no effect on basal release but significantly increased stimulated release. The NMDA receptor antagonist CPP abolished the flurbiprofen-induced potentiation to both modes of stimulation, whilst the metabotropic glutamate receptor antagonist, L-AP3, blocked potassium-stimulated enhancement but had a variable effect on veratridine-stimulated release.