Neurogenic stress is precipitating factor for peptic ulcers. The role of immune cells in that process is not completely studied. The procedures in this study follow the guidelines of the local ethics committee. We used Wistar rats (6 per group) for provocation of neurogenic gastric ulcers (1). Following this, a group of animals was treated each day with antiulcer drug Omeprazole (OME) with dose of 0.8 mg/kg body weight. Animals were sacrificed by decapitation immediately and each day after stress until gastric lesions were present. Lymphocytes from spleen and thymus were isolated. Activity of ornitine decarboxylase (ODC), key regulator of polyamine synthesis, was measured in triplicates(2) to estimate proliferative ability of the cells. All of the data were expressed as mean+/-S.E.M. The significance was calculated using One-Way ANOVA and t-test in STATISTICA 5.0. A decrease in ODC activity in spleen lymphocytes was shown on days 2, 4 and 5 after stress (table 1). More ODC inhibition was observed in OME treated animals during 1-5 days after ulcer provocation. OME injections to unstressed animals resulted in 1.5 fold ODC activation on day 2, but 7- to 11- fold inhibition on the last two days. In thymocytes a 2.8- fold decrease in ODC activity after stress was followed by an increase on days 3 and 4 (table 2). OME treatment resulted in ODC hyperactivation on the first and the last two days. In unstressed animals treated with OME, 2.4- and 5.2- fold increases in this parameter were observed on the first two days. These data reveal different changes in proliferative processes in spleen and thymus lymphocytes during stress ulcer recovery and OME treatment.