Sleep spindles and spike-wave discharges in rats: effects of thalamic lesions

INTRODUCTION The relationship between sleep spindles and spike-wave discharges (SWDs) can be called classical. It was found in humans that in more than 90% of cases studied SWDs occurred in the spindle stage of sleep. Next, sleep spindles could be transformed into SWDs after an injection with penicillin in cats, and benzodiazepines and barbiturates suppress SWDs and enhance sleep spindles while clonidine increase the number of sleep spindles and suppresses SWDs in rats. Finally, it was found that sources and sinks during SWDs and sleep spindles occur at the exact same somatosensory area position, suggesting that the same underlying mechanism controls sleep spindles and SWDs. Outcomes of single-unit and intracellular recordings and surgical isolation studies towards the origin of sleep spindles in cats point towards the thalamus, including the reticular thalamic nucleus (RTN), as the origin of the rhythmic oscillation in the 7-12 Hz range. 6 Recent studies on the origin of SWDs in rats are mainly based on lesion and multiunit recordings. The outcomes of these studies point towards a dual role of the RTN and an intact thalamo-cortico-thalamo circuitry in the generation and spread of these oscillations. Lesions of the lateral thalamus including the RTN in WAG/Rij rats, a genetic model for generalized absence epilepsy, confirmed a pacemaker role of the RTN in rats since a decrease in the number of SWDs was found. These data were interpreted in terms of a functional role of the rostral RTN as being the pacemaker for SWDs, although there were no animals with a completely intact thalamus and a lesioned rostral pole of the RTN. Therefore the functional role of the rostral pole of the RTN in the origin of SWDs still has to be determined. Considering the intimate relation between sleep spindles and SWDs it would be important to establish whether this lesion would also reduce the number of sleep spindles. In the present experiment it was investigated whether lesions of the lateral thalamus including the rostral pole of the RTN would indeed reduce the number of sleep spindles as well as the number of SWDs in rats. If the same pacemaker is involved in the generation of