Development and pathogenetic substantiation of the model of post-traumatic stress disorder

Abstract

The spread of post-traumatic stress disorder (PTSD) among the world's population requires the development of new approaches to the treating of this condition. However, actions in this direction are associated with numerous ethical problems; therefore, there is a need to develop experimental models of PTSD in animals. Existing models of PTSD are based on the idea that this pathology is a consequence of only an acute stress reaction. However, modern views on the pathogenesis of PTSD admit the presence of damage in the brainʹ substrate of psychophysiological processes. The authors set themselves the goal to reconstruct and substantiate a model of PTSD in rats, which would take into account the main pathogenetic mechanisms of this pathology to the greatest extent. Materials and methods. The PTSD model was recreated in white rats and consisted of several components: mild traumatic brain injury and immobilization- cold stress. The research results showed that the reproduction of the PTSD model was accompanied by manifestations of fear, suppression of locomotor activity, emotional arousal and embarrassment, convulsive and chaotic nature of the response to external influences. That is, those damages of the psychophysiological sphere which are characteristic of PTSD are defined. Simultaneously, in the cerebral cortex, ganglion cell discharges, edema of the brain matter, perivascular edema of astrocytes, and neuronophagy phenomena are observed. Changes in metabolism indicate a decrease in the energy supply of transmembrane transport and the nitric oxide cycleʹs intensity. Disturbances in the regulation of metabolic processes were also characterized by an increase in the concentration of uric acid (p <0.001) and a decrease in the content of total protein (p <0.05). On the part of the humoral link of the immune system, signs of the development of inflammatory processes and a weakening of nonspecific defense were established, as evidenced by an increase in the content of circulating immune complexes (p <0.05) and a decrease in the range of heterophilic antibodies (p <0.001). Conclusions. The authors believe that the systemic disorders that occur during the reproduction of the PTSD model have a pathogenetic significance for the developing of this pathology, and the developed model is pathogenetically substantiated.