Neuronal rhythmic activities within thalamocortical circuits range from partially synchronous oscillations during normal sleep to hypersynchrony associated with absence epilepsy. It has been proposed that recurrent inhibition within the thalamic reticular nucleus serves to reduce synchrony and thus prevents seizures. Inhibition and synchrony in slices from mice devoid of the γ-aminobutyric acid type-A (GABA A ) receptor β 3 subunit were examined, because in rodent thalamus, β 3 is largely restricted to reticular nucleus. In β 3 knockout mice, GABA A -mediated inhibition was nearly abolished in reticular nucleus, but was unaffected in relay cells. In addition, oscillatory synchrony was dramatically intensified. Thus, recurrent inhibitory connections within reticular nucleus act as “desynchronizers.”