Sleep deficits and altered sleep features, such as reduced NREM sleep, slow oscillations and sleep spindles are key hallmarks of many neurological disorders. Imaging studies indicate that dysregulation of thalamocortical circuits is associated with sleep abnormalities, but the underlying mechanisms remain poorly understood. Therefore, we studied the impact of thalamic hyperactivity on sleep physiology in rats using chemogenetics.Rats were injected with AAVs to express hM3Dq in either the mediodorsal (MDT), ventroposterior (VPT) or ventromedial thalamus (VMT). Electrodes were implanted in frontal and parietal cortices and the respective thalamic subnuclei. Upon dosing of vehicle or chemogenetic activator DCZ, electrophysiological and accelerometer data was recorded continuously for 22 hours. A separate cohort of rats not expressing hM3Dq was used to control for putative effects of the hM3Dq ligand. Finally, we tested whether increasing GABA-A receptor mediated inhibition preferentially in the thalamus by Gaboxadol or DS-2 could counteract the consequences of thalamic hyperactivity. We found that chemogenetic activation of MDT enhanced light sleep at the expense of deep NREM sleep, reduced sleep spindles and delta-beta oscillations. Conversely, activation of the VPT and VMT increased wakefulness, reduced sleep spindles and delta-beta oscillations during NREM. Neither Gaboxadol nor DS-2 reversed phenotypes driven by VPT or VMT hyperactivity. However, Gaboxadol partially rescued the NREM abnormalities caused by MDT hyperactivity.Our study reveals how hyperactivity of thalamic subnuclei impairs sleep physiology and shows a limited impact of available pharmacology that enhances thalamic inhibition in the investigated circuit models of sleep disruption.