Changes in seizure susceptibility, sleep time and sleep spindles following thalamic and cerebellar lesions.

The present experiment attempted to clarify conflicting evidence on the relationship of sleep spindles to seizure activation. Seizure thresholds were calculated in minutes post-injection following IP administration of the convulsant drug monomethylhydrazine (MMH) to cats with lesions intended to alter the occurrence of spontaneous 12-15 c/sec sleep spindles recorded from sensorimotor cortex. Twelve cats with bilateral cortical and subcortical recording electrodes were divided into 3 groups receiving electrolytic lesions in the dentate nucleus (group I), the ventrobasal (VB) thalamus (group II), or in one of various 'control' regions (group III). Lesion sites in group III animals avoided primary afferent pathways to VB thalamus, destruction of which has been found to enhance sleep spindle activity, and included cerebellar white matter and ventral pontine tegmentum. Prior to the MMH trials, baseline EEGs were obtained during pre- and post-lesion conditions. Following the MMH trial, lesions were verified histologically. Results of the MMH trial revealed that animals with dentate and ventrobasal thalamic lesions showed elevated seizure thresholds and slow wave sleep times relative to their own pre-lesion EEG baselines and to the pre- and post-lesion baselines of control animals. Furthermore, an increased incidence of sleep spindles was associated with dentate lesions while animals with ventrobasal thalamic lesions showed a shift in frequency from 8-11 c/sec to 12-15 c/sec activity during that state. These findings are compatible with the view that sleep spindles do not facilitate seizure activation and may, in fact, exert a protective influence.