The effects of repeated audiogenic convulsions on the organization of sleep in rats

The organization of sleep in Krushinskii-Molodkina rats, with an inherited predisposition to audiogenic convulsions, was studied during and after repeated audiogenic convulsions consisting of two, three, or five relatively rare (separated by intervals of 90 min) or three, five, or nine relatively frequent (separated by intervals of 45 min) generalized clonic-tonic convulsions. In rats subjected to repeated seizures with rare convulsions, behavior in the periods between individual convulsions was dominated by passive waking (75.2 +/- 4.6% of the time), with a low level (24.8 +/- 4.3%) of slow-wave and a complete absence of fast-wave sleep, i.e., there was selective removal of the fast-wave sleep phase from the sleep-waking cycle of the rats. In rats subjected to frequent seizures with frequent convulsions, the period between convulsions showed only passive waking, with complete loss of slow-wave and fast-wave sleep, i.e., total sleep deprivation took place. The minimal latent period before the appearance of the first episodes of slow-wave sleep after repeated convulsions was 59.9 +/- 10.8 min; that for fast-wave sleep was 158.2 +/- 13.4 min. However, the first episodes of slow-wave and fast-wave sleep had an essentially normal structure, though episodes shorter than those in controls were seen, albeit more rarely. Despite the prolonged (up to 7 h) absence of slow-wave sleep during seizures and the prolonged (8.5 h) decrease in fast-wave sleep, there was no compensatory increase in the levels of these states in the sleep-waking cycle during the 12 h of recovery after seizures. Overall, the recovery period after repeated seizures was characterized by an increase (compared with controls) in the total proportion of waking in the behavior of the rats, with a decrease in the total duration of slow-wave and fast-wave sleep. It is concluded that the paroxysmal status significantly disorganizes the operation of the sleep-generating structures of the brain. The functioning of the systems responsible for slow-wave sleep is less affected, while impairments of the activity of the systems responsible for the formation of fast-wave sleep are more significant, affecting primarily the mechanisms triggering this sleep phase.