ВЛИЯНИЕ ПРЕНАТАЛЬНОГО СТРЕССА НА ОКИСЛИТЕЛЬНЫЕ МОДИФИКАЦИИ БЕЛКОВ И АКТИВНОСТЬ СУПЕРОКСИДДИСМУТАЗЫ В МОЗГЕ И ПЛАЗМЕ КРОВИ САМЦОВ КРЫС В МОДЕЛИ ПОСТТРАВМАТИЧЕСКОГО СТРЕССОВОГО РАССТРОЙСТВА
Российский физиологический журнал им И М Сеченова
2 Pavlov Institute of Physiology of the RAS, St. Petersburg, Russia. Biochemical changes during development of posttraumatic stress disorder (PTSD) after prenatal stress were investigated in prenatally stressed male rats. Stress factors activate hypothalamus-pituitary-adrenal (HPA) axis thus increasing penetration of stress hormones into the fetus. It can disturb fetal HPA axis and lead to increased risk of stress-related disorders like PTSD. Our previous works showed that prenatally stressed
... enatally stressed male rats have longer anxious-depressive state in PTSD «stress-restress» model with more severe neuroendocrine disturbances. In this work, oxidative modifications of proteins and superoxide dismutase activity were estimated in the hypothalamus, hippocampus and neocortex of male rats 1, 10 and 20 days after PTSD with and without prenatal stress. Prenatal stress was modeled by 60-min immobilization of females in days 15-19 of pregnancy, and PTSD was modeled with «stress-restress» model consisted of 2-h immobilization, 20-min forced swimming and ether anesthesia with restress in 7 days as 30-min immobilization. Oxidative modification of proteins was measured by amount of products of spontaneous and induced by Fenton's reactive modifications. Prenatally stressed rats without PTSD had increased spontaneous and induced modifications in the hypothalamus -key structure for stress response, and bi-directional changes in superoxide dismutase in neocortex and blood. In prenatally stressed rats, protein oxidation started next day after PTSD induction, but it was found only in the hippocampus. In rats without prenatal stress, protein oxidation started later and was found in all investigated brain structures 10 days after PTSD.