Acute Environmental Hyperthermia Disrupts Cerebral Electrical Activity in Young Male Wistar Rats

Abstract Exposure to extreme environmental temperatures can disturb neural homeostasis and alter brain electrical activity. However, the electrophysiological signatures associated with acute whole-body hyperthermia remain insufficiently characterized. The present study aimed to investigate temperature-induced alterations in electroencephalographic (EEG) activity and associated physiological stress responses in freely moving rats exposed to acute hyperthermia. Male Wistar rats (6–8 weeks old) were exposed to whole-body hyperthermia at 42°C inside a temperature-controlled chamber for up to 4 h or until severe neurological deterioration occurred. EEG signals were continuously recorded and analysed under baseline conditions and during heat exposure. Spectral analysis was performed using artefact-free 2-s epochs across δ, θ, α, β1, and β2 frequency bands. Physiological indicators, including body temperature and plasma corticosterone levels, were measured to assess stress responses. A separate group of rats maintained at 24 ± 1°C served as controls for biochemical comparison. Acute hyperthermia produced significant alterations in EEG spectral dynamics. Power in the θ and α frequency bands increased significantly, whereas δ, β1, and β2 bands showed marked reductions during prolonged heat exposure. The area under the curve of δ and θ bands initially increased but progressively declined with continued thermal stress. These electrophysiological changes were accompanied by significant elevations in core body temperature and corticosterone levels, confirming activation of the physiological stress response. Whole-body hyperthermia induces characteristic EEG spectral alterations that reflect progressive disruption of neural activity under extreme thermal stress. These findings provide insight into the electrophysiological mechanisms of heat-induced neural dysfunction and highlight potential EEG-based markers for monitoring heat stress and predicting adverse neurological outcomes.