Striatal cholinergic receptor activation causes a rapid, selective, & state-dependent rise in corticostriatal β activity.

Cortico-basal ganglia-thalamic (CBT) {beta} oscillations (15-30 Hz) are elevated in Parkinsons disease and correlated with movement disability. To date, no experimental paradigm outside of loss of dopamine has been able to specifically elevate {beta} oscillations in the CBT loop. Here, we show that activation of striatal cholinergic receptors selectively increased {beta} oscillations in mouse striatum and motor cortex. In individuals showing simultaneous {beta} increases in both striatum and M1, {beta} partial directed coherence (PDC) increased from striatum to M1 (but not in the reverse direction). In individuals that did not show simultaneous {beta} increases, {beta} PDC increased from M1 to striatum (but not in the reverse direction), and M1 was characterized by persistent {beta}-HFO phase-amplitude coupling. Finally, the direction of {beta} PDC distinguished between {beta} subbands. This suggests: (1) striatal cholinergic tone exerts state-dependent and frequency-selective control over CBT {beta} power and coordination; (2) ongoing rhythmic dynamics can determine whether elevated {beta} oscillations are expressed in striatum and M1; (3) altered striatal cholinergic tone differentially modulates distinct {beta} subbands.