Increasing concentrations of the anaesthetic agent propofol initially induces sedation before achieving full general anaesthesia. The characteristic changes in electroencephalographic (EEG) rhythms include increased activity in the δ− (1-4 Hz) and α− (8-12 Hz) frequency bands over the frontal region, but increased δ− and decreased α−activity over the occipital region. It is known that the cortex, the thalamus, and the thalamo-cortical feedback loop contribute to some degree to the propofol-induced changes in the EEG power spectrum. However the precise role of each structure to the dynamics of the EEG is unknown. In this paper we apply a neuronal population model of a single thalamo-cortical module to repro-duce the power spectrum changes in EEG during propofol-induced anaesthesia sedation. Based on recent experimental data, the effect of propofol is modelled as an increase in inhibitory synaptic response amplitude and decay time constant in thalamo-cortical relay cells while cortical inhibition is neglected. The model reproduces the power spectrum features observed experimentally both in frontal and occipital electrodes. Moreover a detailed analysis of the model indicates the importance of multiple resting states in brain activity. The work suggests that the α−activity originates from the cortico-thalamic relay interaction, whereas the emergence of δ−activity results from the full cortico-reticular-relay-cortical feedback loop with a prominent enforced thalamic reticular-relay interac-tion. This model suggests an essential role of synaptic GABAergic receptors at relay neurons and, more generally, for the thalamus in the generation of both the α− and the δ−EEG patterns that are seen during propofol anaesthesia sedation.