Abstract
Glucocorticoids arising from chronic stress and long-term inflammatory treatment with corticosteroids are both associated with neuropathology and cognitive impairments. Many previous studies have focused on changes in brain morphology and deficits in learning behavior. However, effects of long-term exposure to stress hormones on electrical brain signaling and sleep-wake patterns have remained largely unexplored. This study aimed to monitor electroencephalographic (EEG) patterns induced by prolonged dexamethasone exposure. Adult male Wistar rats implanted with electrodes on the skull over the frontal and parietal cortices were intraperitoneally injected with either saline or dexamethasone (0.5 mg/kg) once daily for 21 consecutive days. Longitudinal EEG recording was performed on day 6, 11, 16 and 21. Fast Fourier transform was used for frequency power analysis. One-way ANOVA revealed significant increases in parietal EEG power of slow frequencies (delta, theta and alpha) particularly, with the dominant theta activity seen as early as day 11 of dexamethasone treatment. Sleep-wake analysis on day 21 confirmed a significant reduction of rapid-eye movement (REM) sleep and increased slow frequency oscillations mainly in the parietal cortex during the awake period. The number of high-voltage spindles (HVSs) (6-10 Hz EEG oscillation) was significantly increased during awake and slow wave sleep (SWS) periods following dexamethasone treatment. These findings demonstrated that distinct frequency oscillations, sleep-wakefulness and sleep spindles may be parameters of neuropathology produced by long-term dexamethasone exposure. Early detection of these parameters might be predictive of neuropathology in long-term corticosteroid users.
Highlights
Mental and cognitive deficits known as steroid psychosis were found in cases of long‐term an‐ ti‐inflammatory drug treatment (Clark et al, 1952)
All data were nor‐ malized with baseline values obtained before the start of dexamethasone treatment and expressed as percent baseline (% baseline)
The results showed that chron‐ ic dexamethasone exposure significantly decreased the percentage of rapid‐eye movement (REM) sleep
Summary
Mental and cognitive deficits known as steroid psychosis were found in cases of long‐term an‐ ti‐inflammatory drug treatment (Clark et al, 1952). Daily life stress increased corticosterone levels and induced hypothalamic–pituitary–adrenal (HPA) axis hyperactivity, anxiety‐like behavior, impair‐ ments in learning and memory, dysfunction in balance and motor coordination and volume reductions in mul‐. Stress hormones produce neurobiological effects through glucocorticoid receptors generally lo‐ calized in the brain. Sympathoadrenal sys‐ tem hyperactivity is associated with impaired sleep continuity (Hubain et al, 1998). Different brain mech‐ anisms are implicated in sleep disturbances experi‐ enced by people with different mental disorders (Stan‐ er et al, 2003). Many reports have consistently shown that stress hormones can cause impairments in sever‐
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