Atomoxetine Suppresses Astrogliosis in Rats with PTSD and Exposed to Mobile Phone Electromagnetic Waves

Abstract

Introduction: This study investigated the neuroprotective effects of atomoxetine on behavioral and hippocampal histopathological impairments in a rat model of PTSD under prolonged exposure to EMW.

Methods: Twenty-one adult male Wistar rats were allocated to three groups: Naive, control (PTSD+EMW+SAL), and treatment (PTSD+EMW+ATX). The control and treatment groups were exposed to mobile phone electromagnetic waves (EMW) for 44 successive days, with PTSD induced by the single-prolonged stress (SPS) method on day 30. From days 30 to 40, rats received intraperitoneal saline or atomoxetine injections (six times, every other day). Behavioral assessments, including the Open Field Test, Elevated Plus Maze, and Y-Maze, were carried out on days 41–43, followed by hippocampal tissue collection for immunohistochemical and histological analyses. Naive animals received saline injections without EMW exposure or SPS induction and underwent the same behavioral and histological evaluations.

Results: The results of the behavioral tests showed that EMW exposure in PTSD animals exacerbated anxiety disorders and reduced exploratory behaviors. Atomoxetine significantly improved these behavioral deficits. Neuronal counting of H&E-stained hippocampal sections revealed that control animals had a significant reduction in the number of neurons in the CA1 region. GFAP immunohistochemistry revealed a marked increase in astrogliosis. Both alterations were significantly attenuated by atomoxetine treatment.

Conclusion: Atomoxetine attenuates EMW -induced hippocampal injury and astroglial hyperactivity in PTSD rat models, underscoring its potential as a neuroprotective agent that targets both neuronal survival and glial homeostasis. These results suggest the therapeutic value of atomoxetine in hippocampal dysfunction induced by stress and EMW-induced hippocampal dysfunction.