Risk Factors and Mechanisms of Cardiovascular Diseases in Posttraumatic Stress Disorder Model in Wistar Rats as Dependent on Stress Resistance and Age.

The article focuses on the pathogenetic mechanisms of posttraumatic stress disorder (PTSD), which is associated with psychological stress because of the coronavirus pandemic. The molecular mechanisms responsible for disease susceptibility in some individuals and stress resistance in others are amongst crucial research interests of experimental and clinical medicine. Priority data were obtained to indicate that distortions of synthesis and metabolism and, most significantly, a switch between two energy transport forms, glucose and lipids, underlie myocardial dysfunction in young and old stress-sensitive Wistar rats in a PTSD model. Histochemistry and polarization microscopy showed energy deficit in cardiomyocytes and signs of ischemic and hypoxic areas emerging in the myocardium as a result of an accumulation of NADH and NADPH, which initiate excessive production of reactive oxygen species.

Erratum to: "Anxiety and neurometabolite levels in the hippocampus and amygdala after prolonged exposure to predator-scent stress".

Vavilovskii Zhurnal Genetiki i Selektsii = Vavilov Journal of Genetics and Breeding. 2019;23(5):582-587 (in Russian) Page 587, in Acknowledgements instead of The animals and behavioral testing are supported by the budget project (No. 0324-2019-0041). The MRI study is supported by the budget project (No. 0259-2019-0004). All studies are implemented using the equipment of Center for Genetic Resources of Laboratory Animals at ICG SB RAS, supported by the Ministry of Education and Science of Russia (Unique ID# of the project: RFMEFI62117X0015). should read The animals and behavioral testing are supported by the budget project (No. 0324-2019-0041). The MRI study is supported by the budget project (No. 0259-2019-0004). All studies are implemented using the equipment of Center for Genetic Resources of Laboratory Animals at ICG SB RAS, supported by the Ministry of Education and Science of Russia (Unique ID# of the project: RFMEFI62117X0015). The study was conducted within the basic part of the state task of the Ministry of Science and Higher Education of the Russian Federation (No. 17.7255.2017/8.9). The original article can be found under DOI 10.18699/VJ19.528.

Physical Fatigue and Morphofunctional State of the Myocardium in Experimental Chronic Stress.

The relationship between the development of skeletal muscle fatigue of a specific type in male Wistar rats and morphofunctional alterations in the myocardium in the posttraumatic stress disorder (PTSD) model has been investigated for the first time. The aggravation of oxidative stress in the cardiomyocytes and the related transformation of the cell structural components and the depletion of energy reserves in PTSD has been identified as one of the main factors that accelerate the onset of musculoskeletal fatigue.

Behavioral Activity and Some Markers of Posttraumatic Stress Disorder among Serotoninergic System Indicators and Glucocorticoid Metabolizing Enzymes in Rats with Different Duration of Hexenal Sleep.

Post-traumatic stress disorder was imitated in rats with long and short hexenal sleep by exposure to cat odor. Rats with long hexenal sleep demonstrated the highest sensitivity to posttraumatic stress disorders and developed anxiety and depressive disorders. The duration of hexenal sleep correlated with changes in markers of post-traumatic stress disorder, e.g. activity of 11ß-hydroxysteroid dehydrogenase-2 in the liver of non-stressed animals and serotonin and monoamine oxidase A activity in the brain of stressed animals.

Effect of Repeated 1-h Episodes of Immobilization Stress on Activity of Glucocorticoid Metabolism Enzymes in the Liver.

Differences in corticosterone level associated with different activity of glucocorticoid-oxidizing enzymes in the liver were revealed in rats exposed to stress. Pro-inflammatory changes in the liver were associated with enhanced CYP3A-dependent monooxygenation.

Glucocorticoid-Related Regulation of LPO in Brain Cortex during Anxiogenic Stress.

Under conditions of periodic exposures to anxiogenic stress, intensification of LPO in the brain cortex is a glucocorticoid-dependent process. Glucocorticoid receptor antagonist RU38486 prevented increase in monoamine oxidase B activity and content of LPO products of in brain cortex typical of anxiogenic stress. Normalization of LPO intensity under the effect of glucocorticoid receptor antagonist was associated with the correction of stress-induced disturbances.