Abstract
Brain hyperexcitability in sleep apnea is believed to be provoked by hypoxemia, but sleep fragmentation can also play a significant role. Sleep fragmentation can trigger inflammatory mechanisms. The aim of this research was to investigate the effects of chronic sleep fragmentation on seizure susceptibility and brain cytokine profile. Chronic sleep fragmentation in male rats with implanted EEG electrodes was achieved by the treadmill method. Rats were randomized to: treadmill control (TC); activity control (AC) and sleep fragmentation (SF) group. Convulsive behavior was assessed 14 days later by seizure incidence, latency time and seizure severity during 30 min following lindane administration. The number and duration of EEG ictal periods were determined. Levels of IL-1β and IL-6 were measured in the animals' serum and brain structures (hippocampus, thalamus and cerebral cortex), in separate rat cohort that underwent the same fragmentation protocol except lindane administration. Incidence and severity of seizures were significantly increased, while latency was significantly decreased in SF+L compared with TC+L group. Seizure latency was also significantly decreased in SF+L compared to AC+L group. The number and duration of ictal periods were increased in the SF+L compared to the AC+L group. IL-1β was significantly increased in the thalamus, cortex and hippocampus in the SF compared to the AC and TC groups. IL-6 was statistically higher only in the cortex of SF animals, while in the thalamic or hippocampal tissue, no difference was observed between the groups. It could be concluded that fourteen-day sleep fragmentation increases seizure susceptibility in rats and modulates brain production of IL-1β and IL-6. Brain hyperexcitability in sleep apnea is believed to be provoked by hypoxemia, but sleep fragmentation can also play a significant role. Sleep fragmentation can trigger inflammatory mechanisms. The aim of this research was to investigate the effects of chronic sleep fragmentation on seizure susceptibility and brain cytokine profile. Chronic sleep fragmentation in male rats with implanted EEG electrodes was achieved by the treadmill method. Rats were randomized to: treadmill control (TC); activity control (AC) and sleep fragmentation (SF) group. Convulsive behavior was assessed 14 days later by seizure incidence, latency time and seizure severity during 30 min following lindane administration. The number and duration of EEG ictal periods were determined. Levels of IL-1β and IL-6 were measured in the animals’ serum and brain structures (hippocampus, thalamus and cerebral cortex), in separate rat cohort that underwent the same fragmentation protocol except lindane administration. Incidence and severity of seizures were significantly increased, while latency was significantly decreased in SF+L compared with TC+L group. Seizure latency was also significantly decreased in SF+L compared to AC+L group. The number and duration of ictal periods were increased in the SF+L compared to the AC+L group. IL-1β was significantly increased in the thalamus, cortex and hippocampus in the SF compared to the AC and TC groups. IL-6 was statistically higher only in the cortex of SF animals, while in the thalamic or hippocampal tissue, no difference was observed between the groups. It could be concluded that fourteen-day sleep fragmentation increases seizure susceptibility in rats and modulates brain production of IL-1β and IL-6.
Highlights
Sleep fragmentation is defined as a series of brief arousals repeated consecutively throughout the night (Bonnet and Arand, 2003)
There were no seizures in the SFc, ACc and TCc groups, while seizures have been noted in every lin‐ dane‐treated group
The incidence in the sleep fragmentation (SF)+L group was significantly higher compared to the activity control (AC)+L group, with the incidence of 33.33% (Fisher’s exact P=0.0303, Fig. 2), and compared to the treadmill control (TC)+L group, which demonstrated the incidence of 16.67% (Fisher’s exact P=0.0076, Fig. 2)
Summary
Sleep fragmentation is defined as a series of brief arousals repeated consecutively throughout the night (Bonnet and Arand, 2003). This type of fractured sleep causes excessive daytime sleepiness, impaired cogni‐ tion and numerous neurobehavioral deficits (Bonnet and Arand, 2003; Vijayan, 2012). Clinical and transla‐ tional studies suggested certain lifestyle factors may be important modulators of epilepsy, elucidating those related to sleep as important. Shift work and social jetlag caused by modern lifestyles are ac‐ companied by quantitative and qualitative sleep alter‐ ations. An altered sleep pattern has been already rec‐ ognized as a cause of behavioral changes, but recent evidences suggest a bidirectional relationship between the psychiatric illnesses, disrupted circadian rhythm and disrupted sleep (Wulff et al, 2010). Since total sleeping time in fragmented sleep is insignificantly changed, most scientists tend to attribute these conse‐ quences to periodic interruptions and stress (Devinsky et al, 1994)
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