Reduction of adrenergic neurotransmission with clonidine aggravates spike-wave seizures and alters activity in the cortex and the thalamus in WAG/Rij rats.

The alpha-2 adrenoreceptor agonist clonidine in low dose inhibits the release of noradrenaline and aggravates absence seizures. The present study examines properties of two types of spike-wave discharges (SWD) in a genetic model of absence epilepsy, the WAG/Rij rats. After reduction of noradrenergic neurotransmission with clonidine (0.00625 mg/kg, i.p.), the electrical activity was recorded in the neocortex, the ventroposteromedial nucleus (VPM) and the reticular thalamic nucleus (RTN). Clonidine temporally reduced percentage of wakefulness but did not affect sleep. Clonidine decreased the spectral power of sleep EEG (mostly in the delta band), this effect was found in the cortex and in the VPM. Clonidine increased the incidence of SWD type I (generalized); the spectral power of SWD I was lower in the frontal cortex (mostly in 1-9 and 30-100 Hz) and in the VPM (1-5 Hz), but higher in the RTN (9-14 Hz). Local occipital SWD (type II) had a tendency to be less numerous after clonidine, they had a lower power in the 5-9 Hz band in the occipital cortex, in the VPM and in the RTN. It can be concluded that strengthening of 9-14 Hz activity in the RTN may underlie clonidine-induced aggravation of SWD I.