Nikita V. Kudryashov, Alexander A. Gorbunov, Sergey E. Mironov, Dmitriy A. Tikhonov, Andrey A. Nedorubov, Olga Yu. Arshinova, Maria A. Simukhina, Vera N. Busol, Vladimir P. Fisenko

The effect of acute swimming stress, corticosterone, dexamethasone, and fludrocortisone on anxiety-like behavior in mice

Introduction

The effect of acute swimming stress, corticosterone, dexamethasone, and fludrocortisone on anxiety-like behavior in mice. Investigate acute swimming stress, corticosterone, dexamethasone & fludrocortisone's biphasic effects on anxiety-like behavior in mice at 1 & 24 hours.

Abstract

Introduction: Acute swimming stress (ASS) exerts a biphasic effect on anxiety-like behavior (ALB) in mice, inducing an enhancement and a subsequent decrease in ALB 1 h and 24 h after exposure, respectively. Presumably, this effect may be caused by the activation of mineralocorticoid and glucocorticoid receptors, both during the immediate response to acute stress and after its termination at the phase of adaptive changes. Aim of the Research: Comparative study of the effects of acute swimming stress, corticosterone, dexamethasone, and fludrocortisone on ALB in mice 1 h and 24 h after stress exposure or administration of the studied substances. Materials and Methods: To model ASS in adult male ICR mice, the forced swimming test (FST) was employed. ALB was assessed in mice in the open field test 1 h and 24 h after FST or systemic administration of corticosterone (20 mg/kg), dexamethasone (10 mg/kg), and fludrocortisone (0.04 mg/kg). Results: Central activity and anxiety index were increased 1 h after exposure to FST, while an increase in the anxiety index was observed 24 h after exposure to FST in the open field test compared to the non-stressed mice. Corticosterone, dexamethasone, and fludrocortisonedecreased central activity and anxiety index 1 h after the administration, compared to the control group. However, fludrocortisone decreased central activity and total locomotor activity 24 h after administration compared to the control group. Conclusion: A similar pattern of enhancement of anxiety-like behavior was observed in mice 1 h after FST or the administration of corticosterone (single dose 20 mg/kg, i.p.), dexamethasone(single dose 10 mg/kg, i.p.), and fludrocortisone (single dose 0.04 mg/kg, i.p.). Nonetheless, 24 h after exposure to stress or administration of the studied substances, FST decreased ALB, fludrocortisone enhanced ALB, while corticosterone and dexamethasone showed no effect on ALB in mice 24 h after exposure to stress or administration of the studied substances.

Review

This study presents an intriguing investigation into the complex, biphasic effects of acute swimming stress (ASS) on anxiety-like behavior (ALB) in mice, and further explores the roles of key corticosteroids in mediating these responses. The initial premise, suggesting activation of mineralocorticoid and glucocorticoid receptors as a mechanism for both immediate and delayed stress responses, sets a strong theoretical framework. The research aims to comparatively evaluate the effects of ASS, corticosterone, dexamethasone, and fludrocortisone on ALB at two critical time points (1 hour and 24 hours post-exposure/administration), which is a commendable approach to understanding the temporal dynamics of stress and pharmacological interventions. However, a careful review of the abstract reveals significant inconsistencies between the stated introduction, results, and conclusion sections, which critically undermine the clarity and interpretation of the findings. For instance, the introduction posits that ASS induces an enhancement of ALB at 1 hour and a *decrease* at 24 hours. Yet, the results section explicitly states that "an increase in the anxiety index was observed 24 h after exposure to FST" compared to non-stressed mice, directly contradicting the introductory statement. More critically, while the results state that "Corticosterone, dexamethasone, and fludrocortisonedecreased central activity and anxiety index 1 h after the administration," the conclusion then dramatically claims, "A similar pattern of enhancement of anxiety-like behavior was observed in mice 1 h after FST or the administration of corticosterone (...), dexamethasone (...), and fludrocortisone (...)." This fundamental discrepancy regarding the immediate effects of the administered substances (decreasing vs. enhancing anxiety) makes it impossible for the reader to understand the true findings for the 1-hour time point. These contradictions require immediate attention and clarification. While the study appears to offer valuable insights into the differential effects of various corticosteroids and their potential interaction with stress responses over time, particularly the unique effect of fludrocortisone at 24 hours (enhancing ALB), the current presentation of the abstract clouds these contributions. A thorough revision to ensure complete alignment between the stated hypotheses, reported results, and drawn conclusions is essential for this work to fulfill its potential. Once these inconsistencies are resolved, the study's findings on the nuanced temporal regulation of anxiety by stress and different corticosteroid receptor agonists could significantly advance our understanding of stress-related neuropsychiatric disorders.

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