(A) Example traces of electrocorticography (ECoG) and single-unit spiking activity of STN and GPe-Ti neurons during slow-wave activity (SWA) in anaesthetised 6-hydroxydopamine (6-OHDA)-lesioned animals. Note the rhythmic spiking pattern of both neuron types, which either aligns with peaks or troughs of cortical slow (~1 Hz) oscillations. (B) We identified 250 ms epochs of relatively high spiking (>75th percentile) and epochs of low spiking (<25th percentile) based on STN neuron activity during cortical SWA. The distribution of STN (i) and GPe-Ti (ii) spiking activity is shown for one example animal, which confirms that spiking rates are clearly differentiable for the two high and low STN spiking states. GPe-Ti neurons are most active when STN neurons are relatively inactive and vice versa (iii; ***p<.001, Wilcoxon rank-sum test). (C) Average power spectral densities (PSDs) of STN-LFPs in the two states identified above (mean ± SEM, n = 8 animals). The black dotted lines denote the aperiodic fits (exponent values [exp] are colour-coded) for the respective PSDs between 30 and 100 Hz. (D) Aperiodic exponents are high during low STN spiking epochs corresponding to more GPe-Ti activity and, by inference, more inhibition of STN. Inversely, aperiodic exponents are low during high STN spiking epochs associated with less GPe-Ti activity and, by inference, disinhibition (LME: estimate = 0.12, t = 3.92, p<0.001). (E) Average power between 30 and 100 Hz in the STN-LFPs is higher when STN neurons are highly active than when STN spiking is low (LME: estimate = –0.02, t = –2.34, p=0.02). (D, E) Large dots denote the mean per animal and are colour-coded. Small dots denote individual LFP channels. n = 8 animals, *p<0.05, **p<0.01, ***p<.001, LME.