Impact of chronic sleep deprivation and sleep recovery on hippocampal oligodendrocytes, anxiety-like behavior, spatial learning and memory of rats.

Sleep and its quality play an important role in memory, cognition, and quality of life. Sleep deprivation-induced changes in hippocampal neurons and behavior have been studied widely, in contrast, the extent of damage to oligodendrocytes have not been fully understood. The present study aims to investigate chronic sleep deprivation (CSD) and sleep recovery-induced changes in oligodendrocytes of the hippocampus, cognition, and behavior of rats. Male Sprague-Dawley rats (n = 48) were grouped as control, sham control (SC), CSD, and CSD+sleep recovery (CSD+SR) (n = 12/group). CSD and CSD+SR group rats were sleep deprived for 21-days. After CSD, the CSD+SR group rats sleep recovered for 21-days. Oxidative markers, CNPase+ve oligodendrocytes, CNPase intensity, and CNPase gene expression were measured in the hippocampus, and the anxiety-like behavior, spatial learning, and memory were assessed. The 21-days of CSD significantly (p < 0.001) increased oxidative stress and significantly (p < 0.001) reduced the number of CNPase+ve oligodendrocytes, CNPase intensity, and CNPase gene expression when compared to controls. The increased oxidative stress was correlated with reduced CNPase+ve oligodendrocytes, CNPase intensity, and CNPase gene expression (r = -0.9). In-line with cellular changes, an increased (p < 0.01) anxiety-like behavior and impaired spatial memory were observed in the CSD group compared to controls. The 21-days of sleep recovery significantly (p < 0.01) reduced oxidative stress and anxiety-like behavior, improved spatial memory, increased CNPase intensity and CNPase gene expression, and non-significant (p > 0.05) increase in CNPase+ve oligodendrocytes compared to CSD. Overall, the 21-days of CSD reduced the number of CNPase+ve oligodendrocytes in the hippocampus, increased anxiety, and impaired spatial memory in rats. Though the 21-day sleep recovery showed an improvement in all parameters, it was not sufficient to completely reverse the CSD-induced changes to the control level.

Prognostic value of heart rate variability in acute coronary syndrome.

OBJECTIVES: To assess the predictive value of pre-discharge heart rate variability (HRV) parameters in patients with acute coronary syndrome (ACS) treated by percutaneous coronary intervention (PCI). METHODS: 145 consecutive male patients with ACS (aged 57.12 ± 10.81 years) were included in this study. Fifteen minutes electrocardiogram recording was done to measure time-domain [standard deviation of N-N intervals (SDNN), root-mean square differences of successive R-R intervals (rMSSD)] and frequency-domain [low-frequency (LF) power, high-frequency (HF) power and total power (TP)] HRV parameters before and after PCI. The primary end point was the occurrence of major clinical events (MCE) defined as death, sudden death or re-acute myocardial infarction at the end of 3 months follow-up. RESULTS: At a follow-up of 3 months, MCE occurred in 06 patients (4.14%) (Cardiac death was 3.01%, while that of sudden death was 1.13%). Out of six-MCE, four deaths and two re-AMIs occurred. Pre-discharge HRV values (SDNN, rMSSD, TP, LF and HF) were significantly lower in patients with ACS without MCE. Only total power HRV index (AUC=0.748; p=0.040) showed greater prognostic accuracy. CONCLUSIONS: In conclusion, study showed an increase in SDNN, rMSSD, LF, HF and TP after successful revascularization with PCI in patients who had MCE. The resultant sensitivity, specificity of HRV is still limited in the present study. Particularly, its sensitivity is higher (33-83%) with a modest specificity (61-72%).

Effect of chronic sleep deprivation and sleep recovery on hippocampal CA3 neurons, spatial memory and anxiety-like behavior in rats.

Sleep deprivation-induced degenerative changes in the brain lead to the impairment of memory, anxiety, and quality of life. Several studies have reported the effects of sleep deprivation on CA1 and dentate gyrus regions of the hippocampus; in contrast, there is less known about the impact of chronic sleep deprivation (CSD) and sleep recovery on CA3 neurons and behavior. Hence, the present study aimed to understand the effect of CSD and sleep recovery on hippocampal CA3 neurons and spatial memory, and anxiety-like behavior in rats. Sixty male rats (Sprague Dawley) were grouped as control, environmental control (EC), CSD, 5 days sleep recovery (CSD + 5D SR), and 21 days sleep recovery (CSD + 21D SR). CSD, CSD + 5D SR and, CSD + 21D SR group rats were sleep deprived for 21 days (18 h/day). After CSD, the CSD + 5D SR and CSD + 21D SR rats were sleep recovered for 5- and 21-days respectively. Oxidative stress, dendritic arborization of CA3 neurons, spatial memory, and anxiety-like behavior was assessed. Spatial memory, basal, and apical dendritic branching points/intersections in hippocampal CA3 neurons were reduced, and anxiety-like behavior and oxidative stress increased significantly in the CSD group compared to control (p < 0.001). The CSD + 21D SR showed a significant improvement in spatial memory, reduction in anxiety-like behavior, and oxidative stress when compared to the CSD group (p < 0.05). The basal and apical dendritic branching points/intersections in hippocampal CA3 neurons were increased after CSD + 21D SR, however, it was not significant (p > 0.05). Even though the CSD + 21D SR showed a significant improvement in all the parameters, it did not reach the control level. There was an improvement in all the parameters after CSD + 5D SR but this was not significant compared to the CSD group (p > 0.05). Overall results indicate that the CSD-induced impairment of spatial memory and anxiety-like behavior was associated with oxidative stress and reduced dendritic arborization of hippocampal CA3 neurons. The CSD + 21D SR significantly reduced the damage caused by CSD, but it was not sufficient to reach the control level.