Abstract

Emotional stress is considered a serious pathogenetic factor of depression. In this study an ultrasound model of emotional stress developed in our laboratory was applied. It is characterized by the use of ultrasound as the stressor agent. Animals are triggered not by any organic or physical disturbances but by the perception of adverse information. This type of stress can induce depressive-like behavioral changes in rodents, manifested by decreased sucrose preference and increased time of immobility in a forced swim test. Ultrasound stress also increased the levels of oxidative stress markers. This is important, as stress has an established association with increased oxidative processes in the central nervous system. Total glutathione and carbonyl protein content were selected as relevant brain markers, as glutathione plays a critical role in cellular defensive mechanisms during oxidative stress and the level of protein carbonyls can be a measure of global protein oxidation. We demonstrated that two weeks of chronic exposure to ultrasound was enough to cause depressive-like behavioral changes in rats. Increased levels of oxidative stress markers in the hippocampus and prefrontal cortex were also observed after two weeks of such stress. The current study has two goals: the first is to study the relationship of depression and oxidative stress; the second is an additional validation of our approach to modeling stress‑induced depressive-like states in rats. The present data further support the validity of the ultrasound model by expanding information related to the influence of ultrasound stress on behavioral and physiological parameters, which are of great importance in the development of stress-induced depression. A time correlation between the onset of symptoms and a change in the level of oxidative stress markers in the brain is also demonstrated.

Highlights

  • The pathological role of stress in the gen‐ esis of neuropsychiatric disorders including depression is being actively studied

  • In the previous study we showed that the US proto‐ col leads to the development of a depressive‐like stare in rats (Gorlova et al, 2017)

  • Our pilot studies indicated that 24 hours of exposure to 25‐45 kHz did not lead to any behavioral alterations, while 24 hours of exposure to 20‐25 kHz resulted in depressive‐like changes in rats; this period of exposure was not enough to cause stable biochemical changes

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Summary

Introduction

The pathological role of stress in the gen‐ esis of neuropsychiatric disorders including depression is being actively studied. The second group is based on animal models that mimic emotional/psychological stress and relies on naturalistic approaches, such as repeated social defeat (Nestler and Hyman 2010; Chaouloff, 2013), social isolation (Lapiz et al, 2001), hous‐ ing in a deficient cage environment (Baram et al, 2012) or conditions of social instability (Mormède et al, 1990), and aberrant maternal care or deprivation of it (Baram et al, 2012) Some of these paradigms involve pain, inflammation, and noxious elements of a physical nature

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