Increasing concentrations of the anaesthetic agent propofol initially induces sedation before achieving full general anaesthesia. During this state of anaesthesia, the observed specific changes in electroencephalographic (EEG) rhythms comprise increased activity in the δ− (0.5 − 4 Hz) and α− (8 − 13 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 thalamo-cortical neuronal population model to reproduce the power spectrum changes in EEG during propofol-induced anaesthesia sedation. 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 interaction. This model suggests an important role for synaptic GABAergic receptors at relay neurons and, more generally, for the thalamus in the generation of both the δ− and the α− EEG patterns that are seen during propofol anaesthesia sedation.