Central and hormonal mechanisms of adaptation to desynchronization stress

Abstract

The article reports the results of an experiment with male Wistar rats who were subjected to 14-day desynchronization of circadian rhythm. In the first series of experiments, the impact of desynchronization on the levels of collapsin-response mediator protein 2 (CRMP2) in the hypothalamus and epiphysis was examined using a solid-phase indirect ELISA test. An upregulation of CRMP2 in both the hypothalamus and epiphysis was observed. In the second series of experiments, rat behavior was assessed using the elevated plus-maze (EPM) test. As a result, two groups were formed: (1) control group — received inactive CRMP2; (2) experimental group — received CRMP2. Both preparations were administered intranasally 24 hours before and 7 days after desynchronization. After the desynchronization period, rats from both groups were re-tested in the EPM, and the number and duration of specific behavioral acts were recorded. The experimental group showed a three-fold decrease in the number of rearing (p < 0.001) and total duration of grooming (p < 0.001) in the closed arms of the maze, with no change in the number of hanging behaviors, relative to pre-desynchronization levels. The rats then were sacrificed, and serum samples were collected to assess cortisol levels via ELISA. The cortisol level in the experimental group was significantly lower than in the control group (p < 0.001). The study suggests that CRMP2 exhibits anxiolytic activity, helping the organism to adapt to desynchronization stress by influencing circadian rhythm disturbances in specialized brain structures and through hormonal regulation.