Dexamethasone induces alterations of slow wave oscillation, rapid eye movement sleep and high-voltage spindle in rats

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.

Chronic Toxoplasma gondii infection and sleep‐wake alterations in mice

“…Considering the fact that SXT has little effect on cysts as opposed to tachyzoites, the active disseminating form of the parasite, we nonetheless chose to test SXT since Watts et al demonstrated that cysts were in fact active and replicating 36 . On the other hand, we treated mice with Dexamethasone (DXM) seven days in order to access the involvement of inflammation while preventing reactivation of cysts: This length of treatment was reported not to promote sleep‐wake alterations in rats 37 …”

“… 36 On the other hand, we treated mice with Dexamethasone (DXM) seven days in order to access the involvement of inflammation while preventing reactivation of cysts: This length of treatment was reported not to promote sleep‐wake alterations in rats. 37 …”

Dexamethasone induces sleep disturbance in a dose-dependent manner in mice

“…Demisch et al [ 10 ] showed that acute administration of DXM (1 mg) changed the production of nocturnal melatonin (sleep-wake cycle regulator), indicating that steroid-induced sleep disturbance requires only one dose of DXM induction. In the animal model, an administration of 0.5 mg/kg DXM once daily for 21 consecutive days causes an increase in the power of slow EEG frequencies during wake state and decreases the time spent in REM sleep [ 11 ].…”