Striatal cholinergic receptor activation causes a rapid, selective and state-dependent rise in cortico-striatal β activity

Eur J Neurosci. 2018 Oct;48(8):2857-2868. doi: 10.1111/ejn.13906. Epub 2018 Apr 16.

Abstract

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

Keywords: acetylcholine; basal ganglia; motor disorders; oscillations; phase-locking.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.

MeSH terms

  • Animals
  • Beta Rhythm / drug effects
  • Beta Rhythm / physiology*
  • Cholinergic Agonists / pharmacology
  • Corpus Striatum / drug effects
  • Corpus Striatum / metabolism*
  • Female
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Motor Cortex / drug effects
  • Motor Cortex / metabolism*
  • Neural Pathways / drug effects
  • Neural Pathways / metabolism
  • Receptors, Cholinergic / metabolism*
  • Time Factors

Substances

  • Cholinergic Agonists
  • Receptors, Cholinergic