Name:Jonathan Cannon

School/Affiliation:McMaster University

Co-Authors:Jacob Duda

Virtual or In-person:In-person

Abstract:

In fMRI experiments, the basal ganglia is consistently activated by rhythm production. Damage to basal ganglia and alteration of its dopaminergic modulation are experimentally seen to effect rhythm production as well as perception. But what does this circuit actually do during rhythm tasks? We propose that this circuit may specify, maintain, and adapt the tempo with which rhythmic action (e.g. finger tapping or instrument playing) is performed.

As a demonstration, we present a neural population model of the maintenance and change of finger tapping tempo during synchronization and continuation tasks by the cortico-basal-ganglia circuit. Our model builds on existing models of action selection in basal ganglia, but posits that cortico-basal-ganglia loops correspond not just to distinct actions but to a continuum of possible action tempi. A tempo can be “locked in” by dopaminergic modulation in striatum, and during synchronization it can be corrected when synchronization errors suppress dopamine.

The model reproduces the observation in tempo-changing synchronization tasks that tappers make tempo corrections more quickly after large tempo changes than after small changes. When we model Parkinson’s disease as a reduction in striatal dopamine, our model reproduces the increased variation in tapping intervals seen in Parkinsonian patients, and offers insight into the efficacy of rhythmic auditory simulation in supporting rhythmic gait. If experimentally supported, this model would represent a stride forward in our understanding of the neural substrates of rhythm perception/production and would help to make sense of the symptomatology of basal ganglia disorders.