When human divers or experimental animals are exposed to high pressure, they develop brain and biobehavioural disorders. Since it has been demonstrated that pressure exposure increased striatal DA release, the present experiments were intended to investigate whether it resulted from a release in de novo synthesized DA or from a release of DA stores. Free-moving rats implanted with multifibre carbon electrodes sensitive to DA were pretreated with reserpine, a depleter of catecholamine stores, and compressed to 8 MPa. Results show that pretreatment with reserpine had no ability to block the pressure-induced DA release. In the light of previous relevant studies, we suggested that the elevation of DA release under high pressure would be the consequence of a release in de novo synthesized DA.