LAUSR

Cortico‐thalamocortical networks generate sleep spindles and slow waves during non‐rapid eye movement sleep, as well as paroxysmal spike‐wave discharges (i.e. electroencephalogram manifestation of absence epilepsy) and 5–9‐Hz oscillations in genetic rat models (i.e. pro‐epileptic activity). Absence epilepsy is a disorder of the thalamocortical network. We tested a hypothesis that absence epilepsy associates with changes in the slow‐wave activity before the onset of sleep spindles and pro‐epileptic 5–9‐Hz oscillations. The study was performed in the WAG/Rij genetic rat model of absence epilepsy and Wistar rats at the age of 9–12 months. Electroencephalograms were recorded with epidural electrodes from the anterior cortex. Sleep spindles (10–15 Hz), 5–9‐Hz oscillations and their slow‐wave (2–7 Hz) precursors were automatically detected and analysed using continuous wavelet transform. Subjects with electroencephalogram seizures (the “epileptic” phenotype) and without seizure activity (the “non‐epileptic” phenotype) were identified in both strains. It was found that time–amplitude features of sleep spindles and 5–9‐Hz oscillations were similar in both rat strains and in both phenotypes. Sleep spindles in “epileptic” rats were more often preceded by the slow‐wave (~4 Hz) activity than in “non‐epileptic” rats. The intrinsic frequency of slow‐wave precursors of sleep spindles and 5–9‐Hz oscillations in “epileptic” rats was 1–1.5 Hz higher than in “non‐epileptic” rats. In general, our results indicated that absence epilepsy associated with: (a) the reinforcement of slow waves immediately prior to normal sleep spindles; and (b) weakening of amplitude growth in transition “slow wave → spindle/5–9‐Hz oscillation”.