SYNOPSISCentral pain supersensitivity related to depletion of serotonin in the central nervous system has been postulated as a mechanism for migraine. In the present study, transient cerebral ischemia in an animal preparation caused depletion of central nervous system serotonin. Ischemia associated with the prodromal phase of migraine must, therefore, be considered as a possible cause of altered central nervous system serotonin metabolism, possibly leading to increased pain sensitivity.