In rats, damaging key brain areas that control emotions (the septum and amygdala) makes them far less able to handle stress. Giving them a peptide called delta‑sleep‑inducing peptide (DSIP) at a specific dose helped bring back some of that lost stress resistance, improving their behavior, survival, and stress‑related organ changes.

This report describes studies of delta-sleep-inducing peptide in the mechanism of compensating emotional behavior following disruption of a number of structures of the limbic complex (the septum and amygdala). Studies were performed in male Wistar rats. Peptide was given i.p. at a dose of 60 nmol/kg. The individual/typological characteristics of the rats' behavior and their resistance to stress was predicted using an open field test. Emotional stress was modeled by immobilizing the animals and applying electric shocks to the skin. Stress was assessed in terms of survival, adrenal hypertrophy, and thymic involution in stress conditions. Bilateral lesioning to brain structures was carried out by anodic polarization. The results obtained showed that the septum and amygdala play a significant role in the mechanisms of resistance to emotional stress. Bilateral disruption of these structures significantly decreased the animals' resistance to emotional stress, producing alterations in behavior in the open field test, increasing the lethality of acute emotional stress, and inducing changes in stress marker organs (the adrenals and thymus) in stress conditions, as compared to controls. Administration of peptide to animals with lesions to the septum or amygdala increased their resistance to emotional stress, as indicated by open field test behavior, survival, and adrenal and thymus weight in stress conditions. Thus, doses of delta-sleep-inducing peptide partially reverse reductions in stress resistance in animals with lesions to structures of the limbic complex.