An animal model for the evolvement of post-traumatic stress disorder (PTSD) was developed by simulating the hormonal consequences of prolonged stress via the continuous administration of corticosterone by subcutaneously implanted sustained-release pellets. Behavioral, morphological, and biochemical effects were recorded and analyzed. This model has shown cognitive deficits as well as hippocampal damage in the rat similar to those found in PTSD patients. The model was also used to test a therapeutic treatment against stress-induced brain damages. Concomitant treatment with the L-type calcium channel blocker, nimodipine, protected young rats from corticosterone-induced morphological brain changes but not cognitive impairments. The proposed animal model may be useful for testing the efficacy of various neuroprotective drugs. Development of an effective drug treatment for use after a traumatic event and through the trauma period might prevent permanent brain damage and the development of PTSD.