Exposure of rats to platform stress induced a significant elevation in hypothalamic histamine levels. Air blast-stress resulted in a significant increase in hypothalamic histamine concentration and in histidine decarboxylase activity. No significant changes were noted either in the enzyme activity or in histamine levels in the midbrain or cortex of stressed rats. In the nonstressed rats, diphenhydramine (7.5 mg/kg intragastrically), a H1-receptor antagonist, did not influence histidine decarboxylase activity or histamine concentration in any of the three brain regions investigated. However, diphenhydramine pretreatment prevented the increase in histidine decarboxylase activity induced by air blasts. In untreated rats, plasma corticosterone levels were significantly elevated following either platform stress (4.5-fold) or air blasts (7.8-fold). A significant increase was also noted in saline and diphenhydramine-treated animals following these stressors, however, the increase in saline or diphenhydramine treated rats following air blasts was significantly less than that seen in untreated stressed controls.